Clinical and Molecular Hepatology

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Review

Burden of malnutrition and sarcopenia in patients with cirrhosis: pathophysiology, assessment, and management: Takao Miwa, Masahito Shimizu, Bernd Schnabl; Clin Mol Hepatol 2026;32(2):487-510.
Published online December 16, 2025; DOI: https://doi.org/10.3350/cmh.2025.1126

Abstract
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Malnutrition and sarcopenia are highly prevalent and robustly associated with reduced quality of life, disease progression, and poor outcomes, including complications and mortality, in patients with cirrhosis. Their pathophysiology is multifactorial, involving inadequate dietary intake and malabsorption, impaired liver functional reserves, altered energy, protein, and ammonia metabolism, systemic inflammation, hormonal dysregulation, and lifestyle or environmental influences. Despite extensive research, unresolved issues remain regarding optimal diagnostic criteria, as current approaches vary and lack global standardization. Regarding the diagnostic criteria for malnutrition, the usefulness of the Global Leadership Initiative on Malnutrition criteria has been proposed by international nutrition societies. However, evidence supporting their applicability in hepatology remains insufficient. For sarcopenia, differences in disease concept and diagnostic methods among societies indicate that no unified diagnostic standard exists, and clinicians should approach diagnosis with an understanding of the strengths and limitations of each method. Nutritional strategies emphasize adequate energy and protein intake, late evening snacks, and branched-chain amino acid supplementation, while deficiencies in micronutrients require tailored replacement. Nutritional therapy alone has limited effect on sarcopenia, but when combined with exercise it improves muscle mass, physical performance, and outcomes. Comprehensive approaches integrating optimized nutrition, micronutrient support, and structured exercise are essential to alleviate the burden of malnutrition and sarcopenia and to improve prognosis in patients with cirrhosis. This review addresses malnutrition and sarcopenia in cirrhosis by highlighting their prevalence, pathophysiology, clinical impact, and approaches for screening and diagnosis, and by emphasizing personalized nutritional, pharmacological, and exercise interventions to improve patient outcomes.

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Letter: Amino Acid Imbalance Is an Independent Factor for Mortality in Patients With Liver Cirrhosis. Authors' reply
Yuki Utakata, Takao Miwa, Shinji Unome, Naoya Masuda, Mikita Oi, Masashi Aiba, Kenji Imai, Koji Takai, Makoto Shiraki, Naoki Katsumura, Masahito Shimizu
Alimentary Pharmacology & Therapeutics.2026; 63(9): 1329. CrossRef
Covert hepatic encephalopathy as a multi-organ syndrome: the gut–liver–muscle–brain axis, diagnosis, treatment, and multidisciplinary care
Takao Miwa, Cynthia L. Hsu, Masahito Shimizu, Patricia P. Bloom, Bernd Schnabl
Journal of Gastroenterology.2026;[Epub] CrossRef

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Editorial

Rethinking ACLF Prognosis: Can Machine Learning Outperform Conventional Scores? Editorial on: Predictive Machine Learning Model in ICU Patients with Acute-on-Chronic Liver Failure and Two or More Organ Failures: Jung Hee Kim; Received September 15, 2025 Accepted September 17, 2025 Published online September 23, 2025; DOI: https://doi.org/10.3350/cmh.2025.1053 [Accepted]

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Research Letter

Non-contrast magnetic resonance imaging outperforms contrast-enhanced computed tomography in preoperative detection of hepatocellular carcinoma: A paired validation study: Laizhu Zhang, Weiwei Zong, Jialin Gao, Huan Li, Leizhou Xia, Xiaoli Mai, Jun Chen, Binghua Li, Decai Yu; Clin Mol Hepatol 2026;32(1):e34-e37.
Published online September 17, 2025; DOI: https://doi.org/10.3350/cmh.2025.0927

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Editorial

Human cytomegalovirus reactivation in decompensated cirrhosis: marker of immunosuppression or contributor to severity?: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”: Zhujun Cao, Richard Moreau; Clin Mol Hepatol 2026;32(2):953-956.
Published online September 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0962

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Original Article

Predictive machine learning model in intensive care unit patients with acute-on-chronic liver failure and two or more organ failures: Yee Hui Yeo, Mengyi Zhang, Martin S. McCoy, Jian Zu, Yingli He, Yi Liu, Juan Li, Taotao Yan, Yuan Wang, Hirsh D. Trivedi, Ju Dong Yang, Vinay Sundaram, Xiaodan Sun, Zhujun Cao, Chun-Ying Wu, Jonel Trebicka, Fanpu Ji; Clin Mol Hepatol 2025;31(4):1355-1371.
Published online September 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0573

Background/Aims
Prediction of short-term mortality in patients with acute-on-chronic liver failure (ACLF) admitted to the intensive care unit (ICU) may enhance effective management.
Methods
To develop, explain, and validate a predictive machine learning (ML) model for short-term mortality in patients with ACLF with two or more organ failures (OFs). Utilizing a large ICU cohort with detailed clinical information, we identified ACLF patients with two or more OFs according to the EASL-CLIF and NACSELD definitions. ML model was developed for each definition to predict 30-day mortality. The Shapley value was estimated to explain the models. Validation and calibration of these models were performed.
Results
Of 5,994 patients with cirrhosis admitted to ICU, 1,511 met NACSELD criteria, and 1,692 met EASL-CLIF grade II or higher criteria. The CatBoost ACLF (CBA) model had the greatest accuracy in the NACSELD cohort (area under curve [AUC] of 0.87), while the Random Forest ACLF (RFA) model performed best in the EASL-CLIF cohort (AUC of 0.83). Both models showed robust calibration. The models were explained by SHAP score analysis, yielding a rank list, and the top twelve predictors were selected. Both simplified models demonstrated similar performance (CBA model: AUC 0.89, RFA model: AUC 0.81) and significantly outperformed contemporary scoring systems, including CLIF-C ACLF and MELD 3.0. The models were validated in both internal and external cohorts. A simple-to-use online tool was created to predict mortality rates.
Conclusions
We presented explainable, well-validated, and calibrated predictive models for ACLF patients with two or more OFs, which outperformed existing predictive scores.

Citations

Citations to this article as recorded by

Unbiased clustering of acute-on-chronic liver failure patients using machine learning in a real-world ICU cohort
Mengyi Zhang, Fanpu Ji, Jian Zu, Yingli He, Tao Chen, Yi Liu, Hirsh D. Trivedi, Ju Dong Yang, Vinay Sundaram, Yuan Wang, Xiaodan Sun, Zhujun Cao, Chun-Ying Wu, Yee Hui Yeo, Rajiv Jalan
Nature Communications.2026;[Epub] CrossRef
Systematic evaluation of machine learning models for clinical risk prediction on real-world hospital datasets
Qingwen Wu, Ziyou Qi, Qingwei Li, Cuiping Hao, Sujuan Tang
iScience.2026; 29(5): 115654. CrossRef
Navigating the therapeutic tightrope: Precision use of plasmapheresis and continuous renal replacement therapy in liver failure
Manish Manrai, Aditya V Pachisia, Saurabh Dawra, Siddharth Shukla, Atul A Jha
World Journal of Hepatology.2026;[Epub] CrossRef
Beyond the Tipping Point: Advances in the Diagnosis and Management of Acute-on-Chronic Liver Failure and End-Stage Liver Disease
Jonathan Soldera
Diagnostics.2026; 16(10): 1548. CrossRef
Gut–Liver Axis Failure in Critical Alcohol‐Associated Liver Disease: From ICU Secondary Hits to Microbiome‐Targeted Therapy
Yuting Zhang, Yiyu Wang, Yong Yang, Hong Mei, Xinxin Liu, Yuanxiu He, Song Qin, Banghai Feng, Ranjitsinh V. Devkar
Mediators of Inflammation.2026;[Epub] CrossRef

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Letter to the Editor

Plasma lipidomic and fungal signatures predict early mortality in acute liver failure: Yu Ji Kim, Jong-Won Kim; Clin Mol Hepatol 2026;32(1):e21-e23.
Published online August 20, 2025; DOI: https://doi.org/10.3350/cmh.2025.0813

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Research Letter

Early oxidative protein modifications and gut damage/leakiness contribute to drug-induced acute liver failure: Wiramon Rungratanawanich, Ying Qu, Andrew Holmes, Neil Kaplowitz, Byoung-Joon Song; Clin Mol Hepatol 2026;32(1):e29-e33.
Published online August 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0748

Citations

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Tissue-derived extracellular vesicles–mediated delivery of a hepatic enzyme living panorama (HELP) for treating multifactorial liver diseases
Xin Zeng, Wei Jiang, Baohong He, Lan Li, Tian Wu, Fudong Fu, Han Yao, Guangneng Liao, Chengshi Wang, Dongbo Wu
Journal of Nanobiotechnology.2026;[Epub] CrossRef
In silico molecular docking and in vivo evidence of whey protein concentrate-mediated protection against thioacetamide-induced intestinal toxicity in male albino rats via modulation of oxidative stress, inflammation, apoptosis, and fibrosis
Huda Fayez Al-Rashedi, Reem Alenazi, Nashmiah S. Alshammari, Mona A. Ibrahim, Sherif R. Mohamed, Hanan A. Okail
Frontiers in Nutrition.2026;[Epub] CrossRef

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Editorial

Clinical implications of residual changes following HCV clearance: Editorial on “Distinct inflammatory imprint in non-cirrhotic and cirrhotic patients before and after direct-acting antiviral therapy”: So-Young Kim, Eui-Cheol Shin; Clin Mol Hepatol 2026;32(2):935-938.
Published online July 14, 2025; DOI: https://doi.org/10.3350/cmh.2025.0728

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Original Article

Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation: Changze Hong, Zuxiong Huang, Yingli He, Rongqi Wang, Jiaying Lin, Yushan Liu, Baicheng Liu, Xiaoqin Lan, Qinjun He, Wenfan Luo, Qintao Lai, Ling Zhou, Tingting Qi, Yali Ji, Miaoxia Liu, Qiaoping Wu, Yichen Yao, Weihao Liang, Xianbo Wang, Guohong Deng, Yanhang Gao, Yan Huang, Feng Liu, Xiaobo Lu, Zhongji Meng, Yuemin Nan, Hai Li, Beiling Li, Rajiv Jalan, Jinjun Chen; Clin Mol Hepatol 2025;31(4):1316-1332.
Published online July 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0332

Background/Aims
The role of reactivation of human cytomegalovirus (HCMV) in determining outcomes of cirrhotic patients with acute decompensation (AD) is unknown. We aimed to investigate HCMV incidence and potential correlation with hepatic outcomes in AD patients.
Methods
Two prospective multicentre cohorts with AD patients were investigated. Patients in cohort 1 were recruited from 4 centres, while patients in cohort 2 were randomly selected from a second multicentre cohort. HCMV reactivation was established with quantitative real-time polymerase chain reaction assay in seropositive patients.
Results
HCMV reactivation was found in 35 patients from cohort 1 (n=722) and 14 from cohort 2 (n=291), with an incidence of 4.8% in both cohorts. Bacterial infection and liver failure were independently correlated with HCMV reactivation. HCMV reactivation was an independent predictor of 90-day mortality. Among bacterial infection populations in these two cohorts, patients with HCMV reactivation had worse prognosis compared to those without. Incidence of acute-on-chronic liver failure (ACLF) was higher in patients with HCMV reactivation compared to those without and was also independently correlated with development of ACLF. In a total of 49 HCMV reactivation cases, 8 patients were treated with ganciclovir, in whom a significantly lower 90-day mortality compared with those not treated was observed. All 3 patients who underwent liver transplantation with reactivation of HCMV died.
Conclusions
In AD patients, HCMV reactivation was common, especially in those with bacterial infection or liver failure, and they were more prone to having ACLF and 90‑day mortality. The data propose the need for active surveillance for HCMV infection in AD patients.

Citations

Citations to this article as recorded by

Human cytomegalovirus reactivation in decompensated cirrhosis: marker of immunosuppression or contributor to severity?: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Zhujun Cao, Richard Moreau
Clinical and Molecular Hepatology.2026; 32(2): 953. CrossRef
Correspondence to editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Changze Hong, Jinjun Chen
Clinical and Molecular Hepatology.2026; 32(2): e227. CrossRef
Call for preemptive treatment of cytomegalovirus in patients with cirrhosis and acute decompensation: Editorial on “Human cytomegalovirus reactivation in cirrhosis patients with acute decompensation”
Norihiro Imai
Clinical and Molecular Hepatology.2026; 32(2): 949. CrossRef

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Correspondence

Correspondence to editorial on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”: Soon Sun Kim, Hyung Seok Kim, Jae Youn Cheong, Jung Woo Eun; Clin Mol Hepatol 2026;32(1):e72-e74.
Published online April 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0350

Citations

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GULP1: New hope for hepatocellular carcinoma: Reply to correspondence on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Yuhao Xie, Lu-Qi Cao, John Wurpel, Zhe-Sheng Chen
Clinical and Molecular Hepatology.2026; 32(1): e112. CrossRef

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Review

Tracking the trajectory of kidney dysfunction in cirrhosis: the acute kidney injury: chronic kidney disease spectrum: Vishnu Girish, Rakhi Maiwall; Clin Mol Hepatol 2025;31(3):730-752.
Published online March 26, 2025; DOI: https://doi.org/10.3350/cmh.2024.1060

Abstract
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Kidney disease in cirrhosis is now viewed as a continuum encompassing acute kidney injury (AKI), acute kidney disease (AKD), and chronic kidney disease (CKD), rather than three different disorders. Contemporary diagnostic criteria for AKI integrate urine output (UO) parameters and acknowledge the intricate relationship and possibility of overlap between functional and structural as well as acute and chronic entities, including hepatorenal syndrome (HRS). AKI demonstrates a propensity for progression to AKD and CKD, particularly in the context of recurrent and severe insults. The diagnostic complexity is further compounded by limitations in serum creatinine measurements, prompting the integration of novel biomarkers and the need to accurately estimate glomerular filtration rate. The diagnosis, phenotyping, and management of AKI should be prompt and early; the initial step should always be volume and UO assessment. A personalized approach is needed and the possibility of co-existing structural or functional kidney disease should be borne in mind. The earlier concept of waiting for 48 hours to diagnose HRS has evolved and early diagnosis and prompt treatment are advised now. Kidney replacement therapy and simultaneous liver and kidney transplantation may be required in resistant cases.

Citations

Citations to this article as recorded by

Comprehensive Conservative Management Versus Dialysis in Uric Acid Control
Francesca K. Martino, Greta Redi, Marco Bogo, Elena Sgrò, Alessandra Zattarin, Giovanni Samassa, Lucia Federica Stefanelli, Anna Basso, Federico Nalesso
Dietetics.2026; 5(1): 9. CrossRef
Renal Recovery Benefit of Living Versus Deceased Donor Liver Transplantation in Recipients With High Model for End-stage Liver Disease Scores: A Propensity Score-matched Study
Sung-Min Kim, Rak-Kyun Oh, Young-In Yoon, Won-Mook Choi, Shin Hwang, Ki-Hun Kim, Chul-Soo Ahn, Deok-Bog Moon, Tae-Yong Ha, Gi-Won Song, Dong-Hwan Jung, Gil-Chun Park, Sung-Gyu Lee
Transplantation.2026; 110(5): e1016. CrossRef
Early prediction of acute kidney injury after therapeutic paracentesis in decompensated liver cirrhosis: diagnostic value of IL-18, KIM-1, and FGF-23
Ahmed Fayed, Ahmed Ramadan, Tarek Ramzy, Amr Shaker
Renal Failure.2026;[Epub] CrossRef
Risk factors for acute kidney injury in pediatric intensive care units: a systematic review and meta-analysis
Rong Li, Qianqian Yang
BMC Pediatrics.2026;[Epub] CrossRef
Molecular Biomarkers and Risk Prediction Models for Acute Kidney Injury Following Liver Transplantation: A Review
Bing Bin, Yuxiao Chen, Shijian Li, Jihua Wu
Journal of Clinical and Experimental Hepatology.2026; 16(4): 103550. CrossRef
Demographic and regional trends of mortality associated with hepatic cirrhosis and chronic kidney disease, in the United States, 1999-2020: A CDC WONDER database analysis
Mateen Ahmad, Ayman Irshad, Sahaab Noor, Humna Irshad, Muhammad Aliyan Ahmed
Journal of the National Medical Association.2026; 118(3): 525. CrossRef
Uncovering immune dysfunction in ACLF: cellular mechanisms, molecular pathways, and therapeutic frontiers.
Marti Ortega-Ribera, Robert Brenig, Christine Bernsmeier, Gyongyi Szabo
Journal of Hepatology.2026;[Epub] CrossRef
Chronic kidney disease in cirrhosis: a study of inpatients from a global perspective
Florence Wong, Danielle Adebayo, Jacob George, Ramazan Idilman, Peter C Hayes, Mario R Alvares-da-Silva, Aldo Torre, Hailemichael Desalgn Mekonnen, Wai-Kay Seto, Shiv Kumar Sarin, Zhujun Cao, Neil Rajoriya, Aabha Nagral, Henok Fisseha, Anand V Kulkarni, C
Gut.2026; : gutjnl-2025-336802. CrossRef
Association between the C-reactive protein–triglyceride–glucose index (CTI) and the risk of acute kidney injury in critically ill patients with cirrhosis
Lu-Huai Feng, Tianbao Liao, Tingting Su, Xuefei Zhou, Yang Lu, Lina Huang, Zhenhua Yang
BMC Nephrology.2025;[Epub] CrossRef

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Correspondence

Correspondence to letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”: Hyung Seok Kim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun; Clin Mol Hepatol 2026;32(1):e103-e105.
Published online March 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0287

5,764 View
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Reply to Correspondence

Viral hepatitis

Reply to correspondence on “Adverse impact of metabolic dysfunction on fibrosis regression following direct-acting antiviral therapy: A multicenter study for chronic hepatitis C”: Chen-Hua Liu, Yu-Ping Chang; Clin Mol Hepatol 2025;31(2):e232-e233.
Published online February 26, 2025; DOI: https://doi.org/10.3350/cmh.2025.0203

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Original Articles

GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma: Hyung Seok Kim, Jung Hwan Yoon, Ji Yi Choi, Moon Gyeong Yoon, Geum Ok Baek, Minji Kang, Se Ha Jang, Won Park, Yunjin Go, Jestlin Tianthing Ng, Suk Woo Nam, Jee-Yeong Jeong, Ji Eun Han, Hyo Jung Cho, Su Bin Lim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun; Clin Mol Hepatol 2025;31(3):914-934.
Published online February 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.1038

Background/Aims
Hepatocellular carcinoma (HCC) is characterized by high recurrence and mortality, necessitating the identification of reliable biomarkers. In this study, we aimed to identify the predictive gene signatures for HCC recurrence and evaluate the efficiency of GULP PTB domain-containing engulfment adaptor 1 (GULP1) as a predictive and diagnostic marker and therapeutic target for HCC.
Methods
We analyzed genomic datasets from The Cancer Genome Atlas and Gene Expression Omnibus databases via least absolute shrinkage and selection operator Cox regression and 10-fold cross-validation, leading to the development of a 15-gene risk score model, which was validated using three independent datasets. Serum GULP1 and α-fetoprotein levels were assessed to determine the diagnostic accuracy of the model. Using clinical cohorts and patient sera, GULP1 roles were examined, and functional assays in vitro and in vivo were used to evaluate its effects on cell growth, epithelial–mesenchymal transition (EMT), ADP-ribosylation factor 6 (ARF6) activation, and β-catenin signaling.
Results
Our newly developed risk-score model accurately predicted recurrent HCC in all datasets. Among the 15 genes in the risk score model, GULP1 was overexpressed in patients with HCC and independently predicted HCC recurrence. Its expression modulation influenced cell growth and EMT, with observed effects on ARF6 activation and β-catenin signaling pathways.
Conclusions
GULP1 is a crucial biomarker for HCC, serving as a non-invasive diagnostic and predictive tool. It also plays key roles in HCC progression. Our findings highlight the potential use of GULP1 in treatment strategies targeting EMT and HCC recurrence to improve the personalized care and patient outcomes.

Citations

Citations to this article as recorded by

Correspondence to letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Hyung Seok Kim, Soon Sun Kim, Jae Youn Cheong, Jung Woo Eun
Clinical and Molecular Hepatology.2026; 32(1): e103. CrossRef
GULP1, a multifaceted diagnostic biomarker and potential therapeutic target in hepatocellular carcinoma: Editorial on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Yuhao Xie, Lu-Qi Cao, John Wurpel, Zhe-Sheng Chen
Clinical and Molecular Hepatology.2026; 32(1): 413. CrossRef
Letter to the editor on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Juan Yang, Xinyi Li, Sheng Zheng
Clinical and Molecular Hepatology.2026; 32(1): e10. CrossRef
GULP1: New hope for hepatocellular carcinoma: Reply to correspondence on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Yuhao Xie, Lu-Qi Cao, John Wurpel, Zhe-Sheng Chen
Clinical and Molecular Hepatology.2026; 32(1): e112. CrossRef
Correspondence to editorial on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Soon Sun Kim, Hyung Seok Kim, Jae Youn Cheong, Jung Woo Eun
Clinical and Molecular Hepatology.2026; 32(1): e72. CrossRef
Unveiling GULP1 as a hepatocyte-specific role for recurrence: Editorial on “GULP1 as a novel diagnostic and predictive biomarker in hepatocellular carcinoma”
Pengde Lu, Ning Wang
Clinical and Molecular Hepatology.2026; 32(1): 410. CrossRef
Identifying Immunological Biomarkers for Major Depressive Disorder: Insights From Machine Learning, Single‐Nucleus Bioinformatics, and Experimental Validation
Long Kangsheng, Yang Xiaohui, Pei Xin, Ye Yong, Li Hongliang, Deng Yihui, Poorani Gurumallesh Prabu
BioMed Research International.2026;[Epub] CrossRef
MASLD and MASLD-associated HCC: emerging biomarkers and therapeutic avenues
Suki Ha, Xiang Zhang, Lanjuan Li, Jun Yu
Science Bulletin.2026;[Epub] CrossRef
The evolving landscape of biomarkers for systemic therapy in advanced hepatocellular carcinoma
Xinyu Guo, Zhongwei Zhao, Lingyi Zhu, Shuang Liu, Lingling Zhou, Fazong Wu, Shiji Fang, Minjiang Chen, Liyun Zheng, Jiansong Ji
Biomarker Research.2025;[Epub] CrossRef
Advances in research regarding epithelial-mesenchymal transition and prostate cancer
Xi Wei, Rui Liu, Wei Li, Qi Yu, Qing Tao Yang, Tao Li
Frontiers in Cell and Developmental Biology.2025;[Epub] CrossRef
Serum Proteomic Profile Based on the TGF‐β Pathway Stratifies Risk of Hepatocellular Carcinoma
Xiyan Xiang, Kirti Shetty, Herbert Yu, Bibhuti Mishra, Linda L. Wong, Xianghong Jasmine Zhou, Sanjaya K. Satapathy, James M. Crawford, Patricia S. Latham, Steven‐Huy Han, Brandon Mathew, Nabil N. Dagher, Lawrence Lau, Fellanza Cacaj, Anil K. Vegesna, Srin
Liver International.2025;[Epub] CrossRef
Systematic analysis of the expression profiles and prognostic values of the FAM72 family in liver cancer
Weihao Kong, Long Teng, Kangjie Zhang, Yajun Zou, Xingyu Wang, Jianlin Zhang
Biochemistry and Biophysics Reports.2025; 44: 102358. CrossRef

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Direct-acting antiviral therapy for patients with hepatitis C virus-related hepatocellular carcinoma: A nationwide cohort study: Shou-Wu Lee, Sheng-Shun Yang, Pei-Chien Tsai, Chung-Feng Huang, Chi-Yi Chen, Chao-Hung Hung, Chien-Hung Chen, Chi-Ming Tai, Pin-Nan Cheng, Hsing-Tao Kuo, Kuo-Chih Tseng, Lein-Ray Mo, Ching-Chu Lo, Yi-Hsiang Huang, Han-Chieh Lin, Pei-Lun Lee, Ming-Jong Bair, Te-Sheng Chang, Chun-Yen Lin, Szu-Jen Wang, Tsai-Yuan Hsieh, Tzeng-Hue Yang, Cheng-Yuan Peng, Chi-Chieh Yang, Lee-Won Chong, Chien-Wei Huang, Chih-Wen Lin, Cheng-Hsin Chu, Ming-Chang Tsai, Jia-Horng Kao, Chun-Jen Liu, Wan-Long Chuang, Teng-Yu Lee, Ming-Lung Yu, on behalf of TACR investigators; Clin Mol Hepatol 2025;31(3):899-913.
Published online February 5, 2025; DOI: https://doi.org/10.3350/cmh.2024.1015

Background/Aims
The survival benefit of direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) infection in patients with hepatocellular carcinoma (HCC), particularly in Barcelona Clinic Liver Cancer (BCLC) stages B/C, remains largely uncertain. We aimed to explore the impact of DAA therapy on overall survival (OS) in HCC patients using a nationwide cohort study.
Methods
We utilized the nationwide Taiwan Association for the Study of the Liver (TASL) HCV Registry (TACR) database to include all adults receiving a DAA therapy for HCV, excluding those with other viral infections, liver transplantation, non-HCC malignancies, and terminal-staged HCC. We respectively analyzed the adjusted odds ratio (aOR) for sustained virological response (SVR) and adjusted hazard ratio (aHR) for OS.
Results
Between December 2013 and December 2020, 2,205 (9.3%) patients with HCC and 21,569 (90.7%) patients without HCC were include. The SVR rates were 96.6% in the HCC group and 98.8% in the non-HCC group (P<0.001), with HCC being an independent risk factor affecting SVR (aOR 0.41; 95% CI 0.31–0.54; P<0.001). In the whole patient cohort, SVR was independently associated with improved OS (aHR 0.46; 95% CI 0.35–0.60; P<0.001). Among patients with baseline HCC, SVR remained an independent factor related to OS (aHR 0.41; 95% CI 0.28–0.59; P<0.001). The impact of SVR on OS persisted significantly across BCLC stages 0/A and stages B/C.
Conclusions
High SVR rates among HCC patients underscore the importance of DAA therapy in enhancing OS, reaffirming its efficacy across various HCC stages.

Citations

Citations to this article as recorded by

Revisiting unmet needs in clinical research on direct-acting antiviral therapy for HCC patients: Correspondence to letter to the editor on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: A nationwide cohort study”
Teng-Yu Lee, Pei-Chien Tsai, Shou-Wu Lee, Ming- Lung Yu
Clinical and Molecular Hepatology.2026; 32(1): e99. CrossRef
Emerging evidence supports direct-acting antiviral therapy for HCC patients beyond the early stage: Correspondence to editorial on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: A nationwide cohort study”
Teng-Yu Lee, Pei-Chien Tsai, Shou-Wu Lee, Ming-Lung Yu
Clinical and Molecular Hepatology.2026; 32(1): e68. CrossRef
Survival impact of hepatitis C virus eradication in patients with or without active hepatocellular carcinoma: A nationwide cohort study
Teng-Yu Lee, Sheng-Shun Yang, Pei-Chien Tsai, Chung-Feng Huang, Chi-Yi Chen, Chao-Hung Hung, Chien-Hung Chen, Chi-Ming Tai, Pin-Nan Cheng, Hsing-Tao Kuo, Kuo-Chih Tseng, Lein-Ray Mo, Ching-Chu Lo, Yi-Hsiang Huang, Han-Chieh Lin, Pei-Lun Lee, Ming-Jong Bai
European Journal of Cancer.2026; 232: 116109. CrossRef
Letter to the editor on “Direct-acting antiviral therapy for patients with HCV-related hepatocellular carcinoma: a nationwide cohort study”
Qiong Wang, Zhongqing Qian, Xiaodi Yang, Deyan Chen, Xiaojing Wang, Fuliang Chen
Clinical and Molecular Hepatology.2026; 32(1): e7. CrossRef
Setting the Record Straight: Utility and Outcomes in Patients With HCV Related HCC
María Fernanda Guerra‐Veloz, Sital Shah, Beatrice Emmanouil, Mia Olsen, Renita George, Sarah Selemani, Paul J. Ross, Ivana Carey, Neha Mehta, Mark Gillyon‐Powell, Kosh Agarwal
Journal of Viral Hepatitis.2026;[Epub] CrossRef
Letter: Methodological Considerations in Interpreting Polygenic Risk Scores for Hepatocellular Carcinoma After SVR. Authors' Reply
Yu‐Sheng Lin, Yun‐Yu Chen, Teng‐Yu Lee
Alimentary Pharmacology & Therapeutics.2026; 63(10): 1439. CrossRef
Editorial: Residual HCC Risk After Hepatitis C Cure—Can Polygenic Risk Scores Refine Surveillance? Authors' Reply
Yu‐Sheng Lin, Hwai‐I Yang, Teng‐Yu Lee
Alimentary Pharmacology & Therapeutics.2026; 63(10): 1429. CrossRef
Letter: Beyond Association—Operationalising PRS‐5 for Hepatocellular Carcinoma Surveillance. Authors' Reply
Yu‐Sheng Lin, Ying‐Cheng Lin, Teng‐Yu Lee
Alimentary Pharmacology & Therapeutics.2026; 63(10): 1443. CrossRef
HIV, Viral Hepatitis, and Schistosomiasis Association with Liver Cancer: A Systematic Review
Khumbuzile Canham, Pragalathan Naidoo, Sibusiso Senzani, Sayed Shakeel Kader, Zilungile L. Mkhize-Kwitshana
Microorganisms.2025; 13(12): 2753. CrossRef

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Switching to besifovir in patients with chronic hepatitis B receiving tenofovir disoproxil fumarate: A randomized trial: Hyung Joon Yim, Yeon Seok Seo, Ji Hoon Kim, Won Kim, Young Kul Jung, Jae Young Jang, Sae Hwan Lee, Yun Soo Kim, Chang Wook Kim, Hyoung Su Kim, Jae-Jun Shim, Eun-Young Cho, In Hee Kim, Byung Seok Lee, Jeong-Hoon Lee, Byung Seok Kim, Jeong Won Jang, Hyun Woong Lee, Jung Hyun Kwon, Moon Young Kim, Do Seon Song, Jung Gil Park, Yoon Seok Lee, Eileen L. Yoon, Han Ah Lee, Seong Hee Kang, Jin Mo Yang; Clin Mol Hepatol 2025;31(3):810-822.
Published online January 17, 2025; DOI: https://doi.org/10.3350/cmh.2024.0819

Background/Aims
Besifovir (BSV) showed comparable antiviral activity and superior safety profiles to tenofovir disoproxil fumarate (TDF) in treatment-naïve chronic hepatitis B (CHB). However, no data are available regarding the antiviral efficacy and safety of BSV in patients with CHB who switched from long-term TDF to BSV. This study aimed to evaluate the outcome of a 48-week BSV therapy in patients with CHB who switched from long-term TDF treatment.
Methods
In this non-inferiority trial, 153 CHB patients treated with TDF for ≥48 weeks who had hepatitis B virus (HBV) DNA <20 IU/mL were randomized to receive either BSV 150 mg or TDF 300 mg for 48 weeks.
Results
The per-protocol analysis included 130 patients (BSV group, 64; TDF group, 66). The median duration of TDF use before enrollment was 4.14 years. After 48 weeks, 100.0% and 98.5% patients in the BSV and TDF groups, respectively, met the primary endpoint (HBV DNA <20 IU/mL), demonstrating the non-inferior antiviral efficacy of BSV to TDF (95% confidence interval –0.01 to 0.04; P>0.999), with a predefined margin of –0.18. The mean percentage changes in estimated glomerular filtration rates were slightly better in the BSV group (1.67±11.73%) than in the TDF group (–1.24±11.02%). The BSV group showed a significant improvement in bone turnover biomarkers compared to the TDF group; accordingly, hip and spine bone mineral density increased in the BSV group.
Conclusions
In patients with CHB receiving long-term TDF, switching to BSV may improve renal and bone safety with non-inferior antiviral efficacy compared to that of maintaining TDF.

Citations

Citations to this article as recorded by

Correspondence to editorial on “Switching to besifovir in patients with chronic hepatitis B receiving tenofovir disoproxil fumarate: A randomized trial”
Hyung Joon Yim, Seong Hee Kang, Young Kul Jung, Jin Mo Yang
Clinical and Molecular Hepatology.2026; 32(1): e55. CrossRef
Besifovir: a viable option for long-term disease control in chronic hepatitis B: Editorial on “Switching to besifovir in patients with chronic hepatitis B receiving tenofovir disoproxil fumarate: A randomized trial”
Wai-Kay Seto
Clinical and Molecular Hepatology.2026; 32(1): 374. CrossRef
Tenofovir amibufenamide in chronic hepatitis B: Lipid changes and 144-week safety with tenofovir disoproxil fumarate-to-tenofovir amibufenamide switch
Zhi-Hao Zeng, Jin-Qing Liu, Min Zhang, Cai-Liang Qiu, Zhen-Yu Xu
World Journal of Gastroenterology.2025;[Epub] CrossRef

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Plasma lipidomics and fungal peptide-based community analysis identifies distinct signatures for early mortality in acute liver failure: Neha Sharma, Sushmita Pandey, Gaurav Tripathi, Manisha Yadav, Nupur Sharma, Babu Mathew, Abhishak Gupta, Vasundhra Bindal, Sadam H. Bhat, Yash Magar, Rimsha Saif, Sanju Yadav, Amritpal Kaur, Rakhi Maiwall, Shvetank Sharma, Shiv Kumar Sarin, Jaswinder Singh Maras; Clin Mol Hepatol 2025;31(4):1233-1251.
Published online December 13, 2024; DOI: https://doi.org/10.3350/cmh.2024.0554

Background/Aims
Acute liver failure (ALF) has high mortality predominantly due to compromised immune system and increased vulnerability to bacterial and fungal infections.
Methods
Plasma lipidome and fungal peptide-based community (mycobiome) analysis were performed in discovery cohort (ALF=40, healthy=5) and validated in a validation cohort of 230 patients with ALF using high-resolution-mass-spectrometry, artificial neural network (ANN) and machine learning (ML).
Results
Untargeted lipidomics identified 2,013 lipids across 8 lipid group. 5 lipid-species—phosphatidylcholine (PC)[15:0/17:0], PC[20:1/14:1], PC[26:4/10:0], PC[32:0] and TG[4:0/10:0/23:6]—significantly differentiated ALF-NS (FC>10, P<0.05, FDR<0.01). Mycobiome alpha/beta diversity was significantly higher and showed 4 phyla and >20 species significantly dysregulated in ALF-NS linked with lipid metabolism, fatty acid elongation in ER, and others (P<0.05). Lipid and mycobiome diversity values in ALF-NS were strongly correlated (r²>0.7, P<0.05). Multi-modular correlation network showed striking associations between lipid, fungal peptide modules, and clinical parameters specific to ALF-NS (P<0.05). Cryptococcus amylolentus CBS6039 and Penicillium oxalicum 1142 directly correlated with phosphatidylcholine, triglycerides, and severity in ALF-NS (r²>0.85, P<0.05). POD-fungus and POD-lipids showed direct association with infection, necrosis, and hepatic encephalopathy (Beta>1.2, P<0.05). POD-lipid (AUC=0.969 and HR=1.99 [1.02–2.04]) superseded POD-fungus and severity indices for early-mortality prediction. Finally, significant increase in PC (15:0/17:0) level showed highest normalized importance, and ANNs and ML predicted early mortality with >95% accuracy, sensitivity, and specificity. Interestingly, fungal surveillance protein Clec7a was significantly downregulated (>2-fold), leading to a notable increase in fungal infection-mediated choline/phosphatidylcholine and associated enzymes (FC>1.5; Kennedy cycle). This contributed to phosphatidic acid-mediated hyper-inflammation in ALF-NS.
Conclusions
In ALF, the plasma lipidome and mycobiome are dysregulated. Increased circulating phosphatidylcholine could stratify ALF predisposed to early mortality or require emergency liver transplantation.

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Acute-on-chronic liver failure: pathophysiological mechanisms and clinical management
S. K. Sarin, Ashok Choudhury, Anupam Kumar, Nadim Mahmud, G. H. Lee, Qin Ning, Soek-Siam Tan, Kessarin Thanapirom, Vinod Arora, Nobuaki Nakayama, Jun Li, Constantine J. Karvellas
Nature Reviews Gastroenterology & Hepatology.2026; 23(5): 411. CrossRef
Plasma lipidomic and fungal signatures predict early mortality in acute liver failure
Yu Ji Kim, Jong-Won Kim
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Lipidomic profiles associated with treatment related hepatotoxicity in children with acute lymphoblastic leukemia
Emily J. Mason, Jeremy M. Schraw, John P. Woodhouse, M. Monica Gramatges, Kevin J. Williams, Baojiang Chen, Melissa B. Harrell, Olga A. Taylor, Michael E. Scheurer, Philip J. Lupo, Karen R. Rabin, Joanna S. Yi, Van Huynh, Steven D. Mittelman, Etan Orgel,
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Distinct bile mycobiome signature identifies fungal peptide panel predictive for gallbladder carcinoma
Sanju Yadav, Nupur Sharma, Manisha Yadav, Neha Sharma, Gaurav Tripathi, Sadam H. Bhat, Sushmita Pandey, Babu Mathew, Vasundhra Bindal, Rimsha Saifi, Vipul Sharma, Sanyam Falari, Viniyendra Pamecha, Jaswinder Singh Maras
Molecular Therapy Oncology.2026; 34(2): 201220. CrossRef

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Reviews

Liver Transplantation

Prediction and management of small-for-size syndrome in living donor liver transplantation: Jia-hao Law, Alfred Wei-Chieh Kow; Clin Mol Hepatol 2025;31(Suppl):S301-S326.
Published online December 10, 2024; DOI: https://doi.org/10.3350/cmh.2024.0870

Abstract
PDF

Small-for-size syndrome (SFSS) remains a critical challenge in living donor liver transplantation (LDLT), characterized by graft insufficiency due to inadequate liver volume, leading to significant postoperative morbidity and mortality. As the global adoption of LDLT increases, the ability to predict and manage SFSS has become paramount in optimizing recipient outcomes. This review provides a comprehensive examination of the pathophysiology, risk factors, and strategies for managing SFSS across the pre-, intra-, and postoperative phases. The pathophysiology of SFSS has evolved from being solely volume-based to incorporating portal hemodynamics, now recognized as small-for-flow syndrome. Key risk factors include donor-related parameters like age and graft volume, recipient-related factors such as MELD score and portal hypertension, and intraoperative factors related to venous outflow and portal inflow modulation. Current strategies to mitigate SFSS include careful graft selection based on graft-to-recipient weight ratio and liver volumetry, surgical techniques to optimize portal hemodynamics, and novel interventions such as splenic artery ligation and hemiportocaval shunts. Pharmacological agents like somatostatin and terlipressin have also shown promise in modulating portal pressure. Advances in 3D imaging and artificial intelligence-based volumetry further aid in preoperative planning. This review emphasizes the importance of a multifaceted approach to prevent and manage SFSS, advocating for standardized definitions and grading systems. Through an integrated approach to surgical techniques, hemodynamic monitoring, and perioperative management, significant strides can be made in improving the outcomes of LDLT recipients. Further research is necessary to refine these strategies and expand the application of LDLT, especially in challenging cases involving small-for-size grafts.

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Dimitri A Raptis, Leen Alshibi, Sami A Kareem, Sultan Aljudaibi, Massimo Malago, Dieter C Broering
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Zichen Wang, Zhan Qu, Fan Mu, Lexuan Xu, Liangshuo Hu, Bo Wang, Jianhua Shi
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M Tursynbay, M Doskhanov, Z Ospan, B Baimakhanov, S Kaniyev, S Tileuov, D Mukazhanov, A Chormanov
BULLETIN OF SURGERY OF KAZAKHSTAN.2025; 85(4): 73. CrossRef

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Hepatitis E as a trigger for acute-on-chronic liver failure: Maria Buti, Juan Carlos Ruiz-Cobo, Rafael Esteban, Mar Riveiro-Barciela; Clin Mol Hepatol 2025;31(Suppl):S196-S204.
Published online November 11, 2024; DOI: https://doi.org/10.3350/cmh.2024.0758

Abstract
PDF

Acute hepatitis E virus (HEV) infection is typically self-limiting and has a favourable prognosis. However, certain populations such as patients with pre-existing chronic liver disease may experience severe manifestations, including progression to acute-on-chronic liver failure (ACLF). Among viral hepatitis types, hepatitis A, E, and B are major causes of ACLF. Active screening and early diagnosis of HEV infection in patients with cirrhosis, especially those who develop ACLF, can improve management and enable timely antiviral therapy. Preventive measures, including HEV vaccination for high-risk groups, could reduce the morbidity and mortality associated with hepatitis E.

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María Teresa Pérez-Gracia, Lara Martínez-Celdrán, Clara Más-Comes
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Shuangshuang Ma, Qingling Wang, Junjie Lin, Yufeng Gao
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Cholinesterase and the association between hepatic steatosis and liver fibrosis in patients with prior hepatitis E
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Viruses.2026; 18(6): 621. CrossRef
Acute HEV Infection Is a Relevant Cause of Decompensation and ACLF in Patients With Liver Cirrhosis
Katja Dinkelborg, Christian Niehaus, Birgit Bremer, Christine Wundes, Anja Tiede, Natalie Petruch, Katja Deterding, Anke R. M. Kraft, Björn Hartleben, Markus Cornberg, Heiner Wedemeyer, Patrick Behrendt, Benjamin Maasoumy
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Hepatitis A and E Viruses Are Important Agents of Acute Severe Hepatitis in Asia: A Narrative Review
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The role of bacterial outer membrane vesicles in inflammatory response of acute-on-chronic liver failure
Xiaojing Qin, Shuang Wang, Zhanyao Yan, Ninghui Zhao, Jia Yao
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Alba Rabadán Mata, María Dolores Antón Conejero, José María Paredes Arquiola
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Medicina Clínica (English Edition).2025; 165(6): 107187. CrossRef

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Editorials

Steatotic liver disease

Stabilizing hepatic fatty acid oxidation: Editorial on “USP29 alleviates the progression of MASLD by stabilizing ACSL5 through K48 deubiquitination”: Myeung Gi Choi, Na Young Lee, Ja Hyun Koo; Clin Mol Hepatol 2025;31(2):592-595.
Published online November 6, 2024; DOI: https://doi.org/10.3350/cmh.2024.0971

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JAB1/CRL4B complex represses PPARG/ACSL5 expression to promote breast tumorigenesis
Ting Hu, Tianyu Ma, Miaomiao Huo, Jiaxiang Liu, Die Zhang, Yu Li, Jinyuan Chang, Min Zhang, Yinuo Wang, Tianyang Gao, Baowen Yuan, Siqi Wang, Qing Li, Xiaoqi Ma, Jingyao Zhang, Wei Huang, Yan Wang
Cell Death & Differentiation.2026; 33(6): 1175. CrossRef
Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction
Wooyoung Choi, Gun Ha Woo, Tae-Hwan Kwon, Jae-Han Jeon
International Journal of Molecular Sciences.2025; 26(19): 9715. CrossRef

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Hepatocellular carcinoma surveillance after sustained virological response in chronic hepatitis C: Editorial on “Non-invasive prediction of post-sustained virological response hepatocellular carcinoma in hepatitis C virus: A systematic review and meta-analysis”: Ho Soo Chun, Minjong Lee; Clin Mol Hepatol 2025;31(1):261-263.
Published online September 20, 2024; DOI: https://doi.org/10.3350/cmh.2024.0795

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Exploration of Digestive Diseases.2026;[Epub] CrossRef

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Correspondence

Steatotic liver disease

PNPLA3 is one of the bridges between TM6SF2 E167K variant and MASLD: Correspondence to editorial on “TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD”: Baokai Sun, Likun Zhuang; Clin Mol Hepatol 2025;31(1):e67-e69.
Published online September 10, 2024; DOI: https://doi.org/10.3350/cmh.2024.0744

5,375 View
97 Download

Original Articles

Steatotic liver disease

TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD: Baokai Sun, Xiaoqian Ding, Jie Tan, Jie Zhang, Xueru Chu, Shuimi Zhang, Shousheng Liu, Zhenzhen Zhao, Shiying Xuan, Yongning Xin, Likun Zhuang; Clin Mol Hepatol 2024;30(4):863-882.
Published online July 26, 2024; DOI: https://doi.org/10.3350/cmh.2024.0268

Backgrounds/Aims
Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood.
Methods
The Tm6sf2^167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2^167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC).
Results
The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFD-induced Tm6sf2^167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice.
Conclusions
The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.

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Rong Yang, Can Shen, Yu Jia, Yi Yao, Yiheng Zhou, Yu Cheng, Yonglang Cheng, Rui Zeng, Zhi Wan, Qian Zhao, Dongze Li, Xiaoyang Liao
Clinical and Translational Gastroenterology.2026; 17(1): e00949. CrossRef
High-protein diets and metabolic dysfunction-associated steatotic liver disease: A double-edged sword in liver health
Hong-Yuan Yin, Qian-Hui You, Wei-Jie Zhang, Guang Ji, Yan-Qi Dang
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Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models
Jack Leslie, Kishore A. Krishnamurthy, Indresh K. Gopalsamy, Patricia Inacio, Meritxell Huch, Suchira Gallage, Fiona Oakley, Michele Vacca
Nature Reviews Gastroenterology & Hepatology.2026; 23(4): 286. CrossRef
1-O-acetylbritannilactone alleviates high-fat diet-induced fatty liver by covalently targeting NLRP3
Tianyang Jin, Yanni Zhao, Tingxin Xu, Yi Fang, Yaqian Cui, Wenqi Liu, Yongqiang Xiong, Jiaxi Ye, Wu Luo, Bo Hong, Guang Liang, Xiang Hu, Lijiang Huang, Yi Wang
International Immunopharmacology.2026; 174: 116351. CrossRef
Competing Cardiometabolic Pathways of Obesity and Metabolic Dysfunction–Associated Steatotic Liver Disease
Masashi Hirooka, Teruki Miyake, Ryo Yano, Yoshiko Nakamura, Yuki Okazaki, Toyoki Shimamoto, Atsushi Yukimoto, Yasunori Yamamoto, Takao Watanabe, Osamu Yoshida, Kana Hirooka, Yoshio Tokumoto, Masanori Abe, Takeru Iwata, Yoichi Hiasa
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Gang Zhou, Xihan Gu, Xinyao Zhou, Shuai Chen, Hanyang Liu, Jing Wang
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Bojia Li, Shengai Piao, Yin Fu, Qiang Fu, Peiyao Qin, Weitai Kong, Yidi Ma, Zhe Zhang, Xue Fang, Xiaoyang Hu
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Shuo Zhou, Daya Zhang, Runyu Chen, Yan-ting Lv, Da Li, Xianfeng Huang, Fengjiao Mao, Shimei Huang, Shiju Chen, Chen Chen, Ying Mo, Yiping Du, Yuliang Huang, Fan Zeng, Qicen Yao, Feihu Bai
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Zilong Wu, Xinyi Chen, Xiaoying Pan, Kai Luo, Zixiong Zhang, Changyu Zhou, Haibo Wang, Chuying Huang
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Aleksandra Klisic, Ratko Tomašević, Slavko Djuraskovic, Filiz Mercantepe, Ana Ninic
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PNPLA3 is one of the bridges between TM6SF2 E167K variant and MASLD: Correspondence to editorial on “TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD”
Baokai Sun, Likun Zhuang
Clinical and Molecular Hepatology.2025; 31(1): e67. CrossRef
TM6SF2 and PNPLA3: A potential dynamic duo?: Editorial on “TM6SF2 E167K variant decreases PNPLA3-mediated PUFA transfer to promote hepatic steatosis and injury in MASLD”
Andrea Caddeo, Rosellina M. Mancina
Clinical and Molecular Hepatology.2025; 31(1): 293. CrossRef
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Chao Zhang, Tao Yang, Yuan Yu, Qian Jia, Wan-Meng Xiao, Sha Liu, Ze-Hui Yu, Cheng-Li Wen, Yan Wei, Hao Li, Mu-Han Lü
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Mohammad Shafi Kuchay, Narendra Singh Choudhary, Bruno Ramos-Molina
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Indrajit Bhattacharya, Deep Kumar Maity, Amit Kumar, Sampriti Sarkar, Teeshyo Bhattacharya, Amrita Sahu, Remya Sreedhar, Somasundaram Arumugam
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Shuichiro Shiina, Javkhlan Maikhuu, Qing Deng, Terguunbileg Batsaikhan, Lariza Marie Canseco, Maki Tobari, Hitoshi Maruyama, Hiroaki Nagamatsu, Diana Alcantara-Payawal, Rino Gani, Yi-Hsiang Huang, Tawesak Tanwandee, Giovanni Galati, Yoon Jun Kim
Clinical and Molecular Hepatology.2025; 31(3): 671. CrossRef

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372 Download
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Crossref

Viral hepatitis

Vibration-controlled transient elastography for significant fibrosis in treatment-naïve chronic hepatitis B patients: A systematic review and meta-analysis: Mi Na Kim, Jihyun An, Eun Hwa Kim, Hee Yeon Kim, Han Ah Lee, Jung Hwan Yu, Young-Joo Jin, Young Eun Chon, Seung Up Kim, Dae Won Jun, Ji Won Han, Miyoung Choi; Clin Mol Hepatol 2024;30(Suppl):S106-S116.
Published online July 23, 2024; DOI: https://doi.org/10.3350/cmh.2024.0371

Backgrounds/Aims
Accurate diagnosis of significant liver fibrosis in patients with chronic hepatitis B (CHB) is crucial when determining whether to initiate antiviral treatment (AVT). We conduct a meta-analysis to assess the diagnostic performance of vibration-controlled transient elastography (VCTE) for significant liver fibrosis in AVT-naïve CHB patients with serum alanine transaminase (ALT) levels within 5-fold the upper limit of normal (ULN).
Methods
The Ovid-Medline, EMBASE, Cochrane, and KoreaMed databases were searched to identify studies that compared the performance of VCTE and liver biopsy (reference standard) when diagnosing significant liver fibrosis (≥F2) in AVT-naïve CHB patients with ALT within 5-fold the ULN. A hierarchical summary receiver operating characteristic curve (HSROC) and bivariate model were performed to evaluate the diagnostic performance of VCTE in the meta-analysis.
Results
Eight studies (2,003 patients) were included. The summary sensitivity and specificity for diagnosis of significant liver fibrosis were 0.78 (95% confidence interval [CI], 0.66–0.86) and 0.72 (95% CI, 0.60–0.82), respectively. The HSROC for the diagnosis of significant liver fibrosis was 0.81 (95% CI, 0.72–0.86). The optimal cutoff value of VCTE for diagnosis of significant liver fibrosis was 7.7 kPa with a sensitivity of 0.64 (95% CI, 0.50–0.76) and specificity of 0.83 (95% CI, 0.72–0.90).
Conclusions
Our study demonstrated that VCTE has an acceptable diagnostic performance for significant liver fibrosis in AVT-naïve CHB patients with ALT within 5-fold the ULN.

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Acute liver injury and Acute liver failure

Correspondence to editorial on “Dynamic analysis of acute deterioration in chronic liver disease patients using modified quick sequential organ failure assessment”: Do Seon Song, Dong Joon Kim; Clin Mol Hepatol 2024;30(4):1012-1015.
Published online June 18, 2024; DOI: https://doi.org/10.3350/cmh.2024.0448

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Editorial

Acute liver injury and Acute liver failure

Modified quick-SOFA score: Can it enhance prognostic assessment for hospitalized patients with chronic liver diseases?: Editorial on “Dynamic analysis of acute deterioration in chronic liver disease patients using modified quick sequential organ failure assessment”: Simone Incicco, Salvatore Piano; Clin Mol Hepatol 2024;30(4):695-697.
Published online June 3, 2024; DOI: https://doi.org/10.3350/cmh.2024.0409

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Original Article

Acute liver injury and Acute liver failure

Dynamic analysis of acute deterioration in chronic liver disease patients using modified quick sequential organ failure assessment: Do Seon Song, Hee Yeon Kim, Young Kul Jung, Tae Hyung Kim, Hyung Joon Yim, Eileen L Yoon, Ki Tae Suk, Jeong-ju Yoo, Sang Gyune Kim, Moon Young Kim, Young Chang, Soung Won Jeong, Jae Young Jang, Sung-Eun Kim, Jung-Hee Kim, Jung Gil Park, Won Kim, Jin Mo Yang, Dong Joon Kim, Korean Acute-on-Chronic Liver Failure (KACLiF) study group, Ashok Kumar Choudhury, Vinod Arora, Shiv Kumar Sarin, APASL ACLF Research Consortium (AARC) for APASL ACLF working party; Clin Mol Hepatol 2024;30(3):388-405.
Published online April 11, 2024; DOI: https://doi.org/10.3350/cmh.2023.0563

Background/Aims
Quick sequential organ failure assessment (qSOFA) is believed to identify patients at risk of poor outcomes in those with suspected infection. We aimed to evaluate the ability of modified qSOFA (m-qSOFA) to identify high-risk patients among those with acutely deteriorated chronic liver disease (CLD), especially those with acute-onchronic liver failure (ACLF).
Methods
We used data from both the Korean Acute-on-Chronic Liver Failure (KACLiF) and the Asian Pacific Association for the Study of the Liver ACLF Research Consortium (AARC) cohorts. qSOFA was modified by replacing the Glasgow Coma Scale with hepatic encephalopathy, and an m-qSOFA ≥2 was considered high.
Results
Patients with high m-qSOFA had a significantly lower 1-month transplant-free survival (TFS) in both cohorts and higher organ failure development in KACLiF than those with low m-qSOFA (Ps<0.05). Subgroup analysis by ACLF showed that patients with high m-qSOFA had lower TFS than those with low m-qSOFA. m-qSOFA was an independent prognostic factor (hazard ratios, HR=2.604, 95% confidence interval, CI 1.353–5.013, P=0.004 in KACLiF and HR=1.904, 95% CI 1.484– 2.442, P<0.001 in AARC). The patients with low m-qSOFA at baseline but high m-qSOFA on day 7 had a significantly lower 1-month TFS than those with high m-qSOFA at baseline but low m-qSOFA on day 7 (52.6% vs. 89.4%, P<0.001 in KACLiF and 26.9% vs. 61.5%, P<0.001 in AARC).
Conclusions
Baseline and dynamic changes in m-qSOFA may identify patients with a high risk of developing organ failure and short-term mortality among CLD patients with acute deterioration.

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Viral hepatitis

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Viral hepatitis

Toward hepatitis C virus elimination using artificial intelligence: Moon Haeng Hur, Jeong-Hoon Lee; Clin Mol Hepatol 2024;30(2):147-149.
Published online February 23, 2024; DOI: https://doi.org/10.3350/cmh.2024.0135

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Review

Steatotic liver disease

Taiwan Association for the Study of the Liver-Taiwan Society of Cardiology Taiwan position statement for the management of metabolic dysfunction- associated fatty liver disease and cardiovascular diseases: Pin-Nan Cheng, Wen-Jone Chen, Charles Jia-Yin Hou, Chih-Lin Lin, Ming-Ling Chang, Chia-Chi Wang, Wei-Ting Chang, Chao-Yung Wang, Chun-Yen Lin, Chung-Lieh Hung, Cheng-Yuan Peng, Ming-Lung Yu, Ting-Hsing Chao, Jee-Fu Huang, Yi-Hsiang Huang, Chi-Yi Chen, Chern-En Chiang, Han-Chieh Lin, Yi-Heng Li, Tsung-Hsien Lin, Jia-Horng Kao, Tzung-Dau Wang, Ping-Yen Liu, Yen-Wen Wu, Chun-Jen Liu; Clin Mol Hepatol 2024;30(1):16-36.
Published online October 4, 2023; DOI: https://doi.org/10.3350/cmh.2023.0315

Abstract
PDF

Metabolic dysfunction-associated fatty liver disease (MAFLD) is an increasingly common liver disease worldwide. MAFLD is diagnosed based on the presence of steatosis on images, histological findings, or serum marker levels as well as the presence of at least one of the three metabolic features: overweight/obesity, type 2 diabetes mellitus, and metabolic risk factors. MAFLD is not only a liver disease but also a factor contributing to or related to cardiovascular diseases (CVD), which is the major etiology responsible for morbidity and mortality in patients with MAFLD. Hence, understanding the association between MAFLD and CVD, surveillance and risk stratification of MAFLD in patients with CVD, and assessment of the current status of MAFLD management are urgent requirements for both hepatologists and cardiologists. This Taiwan position statement reviews the literature and provides suggestions regarding the epidemiology, etiology, risk factors, risk stratification, nonpharmacological interventions, and potential drug treatments of MAFLD, focusing on its association with CVD.

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Hepatic neoplasm

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Review

Acute liver injury and Acute liver failure

Acute-on-chronic liver failure: Terminology, mechanisms and management: Vinay Kumar BR, Shiv Kumar Sarin; Clin Mol Hepatol 2023;29(3):670-689.
Published online March 20, 2023; DOI: https://doi.org/10.3350/cmh.2022.0103

Abstract
PDF

Acute-on-chronic liver failure is an acute deterioration of liver function manifesting as jaundice and coagulopathy with the development of ascites, with a high probability of extrahepatic organ involvement and high 28-day mortality. The pathogenesis involves extensive hepatic necrosis, which is associated with severe systemic inflammation and subsequently causes the cytokine storm, leading to portal hypertension, organ dysfunction, and organ failure. These patients have increased gut permeability, releasing lipopolysaccharide (LPS) and damage-associated molecular patterns (DAMPS) in the blood, leading to hyper-immune activation and the secretion of cytokines, followed by immune paralysis, causing the development of infections and organ failure in a proportion of patients. Early detection and the institution of treatment, especially in the "Golden Window" period of 7 days, gives an opportunity for reversal of the syndrome. Scores like the Asian Pacific Association for the Study of the Liver (APASL) ACLF research consortium (AARC) score, a model for end stage liver disease (MELD), and the CLIF Consortium acute-on-chronic liver failure (CLIF-C ACLF) score can help in the prediction of mortality. Treatment strategy includes treatment of acute insult. Patients should be considered for early transplant with MELD score >28, AARC score >10, high-grade hepatic encephalopathy, and in the absence of >2 organ failure or overt sepsis to improve survival of up to 80% at five years. Patients, with no option of transplant, can be treated with emerging therapies like faecal microbial transplant, plasma exchange, etc., which need further evaluation.

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Original Article

Decreased vitamin D-binding protein level portends poor outcome in acute-on-chronic liver failure caused by hepatitis B virus: Daxian Wu, Qunfang Rao, Zhongyang Xie, Xiaoqing Zhu, Yuanmei Che, Jian Wu, Hainv Gao, Jingyu Zhang, Zhouhua Hou, Xiaoyu Cheng, Zeyu Sun; Clin Mol Hepatol 2022;28(4):912-925.
Published online July 28, 2022; DOI: https://doi.org/10.3350/cmh.2022.0121

Background/Aims
Acute-on-chronic liver failure (ACLF) is a catastrophic illness. Few studies investigated the prognostic value of vitamin D-binding protein (VDBP) for hepatitis B virus (HBV)-related ACLF (HBV-ACLF) resulted in conflicting results.
Methods
Two prospective HBV-ACLF cohorts (n=287 and n=119) were enrolled to assess and validate the prognostic performance of VDBP.
Results
VDBP levels in the non-survivors were significantly lower than in the survivors (P<0.001). Multivariate Cox regression demonstrated that VDBP was an independent prognostic factor for HBV-ACLF. The VDBP level at admission gradually decreased as the number of failed organs increased (P<0.001), and it was closely related to coagulation failure. The areas under the receiver operating characteristic curve (AUCs) of the Child-Pugh-VDBP and chronic liver failuresequential organ failure assessment (CLIF–SOFA)-VDBP scores were significantly higher than those of Child-Pugh (P<0.001) and CLIF-SOFA (P=0.0013). The AUCs of model for end-stage liver disease (MELD)-VDBP were significantly higher than those of MELD (P= 0.0384) only in the case of cirrhotic HBV-ACLF patients. Similar results were validated using an external multicenter HBV-ACLF cohort. By longitudinal observation, the VDBP levels gradually increased in survivors (P=0.026) and gradually decreased in non-survivors (P<0.001). Additionally, the VDBP levels were found to be significantly decreased in the deterioration group (P=0.012) and tended to be decreased in the fluctuation group (P=0.055). In contrast, they showed a significant increase in the improvement group (P=0.036).
Conclusions
The VDBP was a promising prognostic biomarker for HBV-ACLF. Sequential measurement of circulating VDBP shows value for the monitoring of ACLF progression.

Citations

Citations to this article as recorded by

Vitamin D deficiency in chronic hepatitis B across the disease spectrum: association with viral activity rather than hepatocellular carcinoma
Dr Tufael, Abu Bakar Siddique, Md Haroon Or Rashid, Mohd Hasan Mujahid, Nabil Deb Nath, Asim Debnath, Most Farhana Akter, Md. Robiul Islam, Vijay Jagdish Upadhye
BMC Gastroenterology.2026;[Epub] CrossRef
Omics in acute‐on‐chronic liver failure
Peng Li, Xi Liang, Jinjin Luo, Jun Li
Liver International.2025;[Epub] CrossRef
Deficiency of vitamin D-binding protein exacerbates liver fibrosis by disrupting iron homeostasis via the activation of YAP signaling
Qing Zheng, Qingquan Tan, Dan Wang, Yanling Ma, Yanni Zhou, Yonghua Chen, Dan Long, Jiayin Yang, Li Feng
Experimental Cell Research.2025; 452(2): 114767. CrossRef
miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1
Feiyue Xie, Qiuping Ren, Jun He, Menghang Wu
Hereditas.2025;[Epub] CrossRef

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Snapshot

Liver fibrosis, cirrhosis, and portal hypertension

Acute on chronic liver failure in cirrhosis: Marta Tonon, Salvatore Piano; Clin Mol Hepatol 2022;28(2):273-275.
Published online February 14, 2022; DOI: https://doi.org/10.3350/cmh.2022.0036

Citations

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From Liver to Brain: A 2.5D Deep Learning Model for Predicting Hepatic Encephalopathy Using Opportunistic Non-contrast CT in Hepatitis B Related Acute-on-Chronic Liver Failure Patients
Zonglin Liu, Xueyun Zhang, Ying Chen, Qi Zhang, Zhenxuan Ma, Yue Wu, Yuxin Huang, Yajie Li, Xi Zhao, Wenchao Gu, Jiaxing Wu, Ying Tao, Yuxin Shi, Zhenwei Yao, Yan Ren, Yuxian Huang, Shiman Wu
Journal of Imaging Informatics in Medicine.2026;[Epub] CrossRef
Outcomes of Highly Urgent ABO-Incompatible Living Donor Liver Transplantation in National Databases
Jongman Kim, Sang Jin Kim, Boram Park, Kyunga Kim, YoungRok Choi, Geun Hong, Jun Yong Park, Young Seok Han, Nam-Joon Yi, Seung Heui Hong, Soon-Young Kim, Jungbun Park, Youngwon Hwang, Dong-Hwan Jung
Journal of Korean Medical Science.2026;[Epub] CrossRef
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Jongman Kim
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RAC1 as a novel therapeutic target for acute liver failure
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Frontiers in Microbiology.2023;[Epub] CrossRef

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Original Article

Liver fibrosis, cirrhosis, and portal hypertension

Galectin-3 inhibits cardiac contractility via a tumor necrosis factor alpha-dependent mechanism in cirrhotic rats: Ki Tae Yoon, Hongqun Liu, Jing Zhang, Sojung Han, Samuel S. Lee; Clin Mol Hepatol 2022;28(2):232-241.
Published online January 5, 2022; DOI: https://doi.org/10.3350/cmh.2021.0141

Background/Aims
Galectin-3 plays a key pathogenic role in cardiac hypertrophy and heart failure. The present study aimed to investigate the effects of galectin-3 on cardiomyopathy – related factors and cardiac contractility in a rat model of cirrhotic cardiomyopathy.
Methods
Rats were divided into two sets, one for a functional study, the other for cardiac contractile-related protein evaluation. There were four groups in each set: sham operated and sham plus N-acetyllactosamine (N-Lac, a galectin-3 inhibitor; 5 mg/kg); bile duct ligated (BDL) and BDL plus N-Lac. Four weeks after surgery, ventricular level of galectin-3, collagen I and III ratio, tumor necrosis factor alpha (TNFα), and brain natriuretic peptide (BNP) were measured either by Western blots or immunohistochemistry or enzyme-linked immunosorbent assay. Blood pressure was measured by polygraph recorder. Cardiomyocyte contractility was measured by inverted microscopy.
Results
Galectin-3 and collagen I/III ratio were significantly increased in cirrhotic hearts. TNFα and BNP were significantly increased in BDL serum and heart compared with sham controls. Galectin-3 inhibitor significantly decreased galectin-3, TNFα, and BNP in cirrhotic hearts but not in sham controls. N-Lac also significantly improved the blood pressure, and systolic and diastolic cardiomyocyte contractility in cirrhotic rats but had no effect on sham controls.
Conclusion
Increased galectin-3 in the cirrhotic heart significantly inhibited contractility via TNFα. Inhibition of galectin-3 decreased the cardiac content of TNFα and BNP and reversed the decreased blood pressure and depressed contractility in the cirrhotic heart. Galectin-3 appears to play a pathogenic role in cirrhotic cardiomyopathy.

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Review

Viral hepatitis

Approaches to quantifying hepatitis B virus covalently closed circular DNA: Henrik Zhang, Thomas Tu; Clin Mol Hepatol 2022;28(2):135-149.
Published online October 22, 2021; DOI: https://doi.org/10.3350/cmh.2021.0283

Abstract
PDF

Chronic hepatitis B is a major cause of liver disease worldwide and is currently incurable. Hepatitis B virus (HBV) covalently closed circular (ccc) DNA is a key form of the virus responsible for its persistence and is the transcriptional template for all viral transcripts. The field is focussed on methods to clear HBV cccDNA but this been limited by technical difficulties in its quantification due to: identical sequence to other forms of HBV DNA; low copy number per cell; and high resistance to denaturation by heat, leading to difficulty using polymerase chain reaction or hybridization methods for detection. A number of assays have been developed in order to overcome these hurdles either directly or detecting cccDNA levels indirectly via its transcriptional products. In this review, we summarize the approaches to cccDNA quantification that are currently used, and outline key open questions in the cccDNA biology field which remain to be answered due to the limitations of current methods.

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Letter to the Editor

Hepatic neoplasm

Impact of branched-chain amino acids and frailty on the management of lenvatinib-related fatigue in patients with hepatocellular carcinoma: Shigeo Shimose, Shunji Koya, Takumi Kawaguchi, Keisuke Hirota, Sachiyo Yoshio, Takashi Niizeki, Hiroo Matsuse, Takuji Torimura; Clin Mol Hepatol 2021;27(4):616-619.
Published online September 13, 2021; DOI: https://doi.org/10.3350/cmh.2021.0258

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Editorials

Hepatic neoplasm

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Published online October 1, 2020; DOI: https://doi.org/10.3350/cmh.2020.0220

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Acute liver injury and Acute liver failure

Acute-on-chronic liver failure: A predictor of poor prognosis in patients with variceal bleeding or a risk factor for variceal bleeding?: Nae-Yun Heo; Clin Mol Hepatol 2020;26(4):487-488.
Published online October 1, 2020; DOI: https://doi.org/10.3350/cmh.2020.0209

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Original Article

Acute liver injury and Acute liver failure

Acute-on-chronic liver failure as a major predictive factor for mortality in patients with variceal bleeding: Jongbeom Shin, Jung Hwan Yu, Young-Joo Jin, Hyung Joon Yim, Young Kul Jung, Jin Mo Yang, Do Seon Song, Young Seok Kim, Sang Gyune Kim, Dong Joon Kim, Ki Tae Suk, Eileen L. Yoon, Sang Soo Lee, Chang Wook Kim, Hee Yeon Kim, Jae Young Jang, Soung Won Jeong, on Behalf of the Korean Acute-onChronic Liver Failure (KACLiF) Study Group; Clin Mol Hepatol 2020;26(4):540-553.
Published online September 17, 2020; DOI: https://doi.org/10.3350/cmh.2020.0034

Background/Aims
This study examined the risk factors associated with mortality in cirrhotic patients hospitalized with variceal bleeding, and evaluated the effects of acute-on-chronic liver failure (ACLF) on the prognosis of these patients.
Methods
This study was retrospectively conducted on patients registered in the Korean acute-on-chronic liver failure study cohort, and on 474 consecutive cirrhotic patients hospitalized with variceal bleeding from January 2013 to December 2013 at 21 university hospitals. ACLF was defined as described by the European Association for the Study of Liver-Chronic Liver Failure Consortium.
Results
Among a total of 474 patients, 61 patients were diagnosed with ACLF. The cumulative overall survival (OS) rate was lower in the patients with ACLF than in those without (P<0.001), and patients with higher ACLF grades had a lower OS rate (P<0.001). The chronic liver failure-sequential organ failure assessment (CLIF-SOFA) score was identified as a significant prognostic factor in patients hospitalized with variceal bleeding (hazard ratio [HR], 1.40; 95% confidence interval [CI], 1.30–1.50; P<0.001), even in ACLF patients with variceal bleeding (HR, 1.32; 95% CI, 1.19–1.46, P<0.001). Concerning the prediction of the mortality risk at 28- and 90-day using CLIF-SOFA scores, c-statistics were 0.895 (95% CI, 0.829–0.962) and 0.897 (95% CI, 0.842–0.951), respectively, and the optimal cut-off values were 6.5 and 6.5, respectively.
Conclusions
In cirrhotic patients hospitalized with variceal bleeding, the prognosis was poor when accompanied by ACLF, especially depending upon CLIF-SOFA score. CLIF-SOFA model well predicted the 28-day or 90-day mortality for cirrhotic patients who experienced variceal bleeding.

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Review

Steatotic liver disease

Precision medicine in nonalcoholic fatty liver disease: New therapeutic insights from genetics and systems biology: Silvia Sookoian, Carlos J. Pirola; Clin Mol Hepatol 2020;26(4):461-475.
Published online September 10, 2020; DOI: https://doi.org/10.3350/cmh.2020.0136

Despite more than two decades of extensive research focusing on nonalcoholic fatty liver disease (NAFLD), no approved therapy for steatohepatitis—the severe histological form of the disease—presently exists. More importantly, new drugs and small molecules with diverse molecular targets on the pathways of hepatocyte injury, inflammation, and fibrosis cannot achieve the primary efficacy endpoints. Precision medicine can potentially overcome this issue, as it is founded on extensive knowledge of the druggable genome/proteome. Hence, this review summarizes significant trends and developments in precision medicine with a particular focus on new potential therapeutic discoveries modeled via systems biology approaches. In addition, we computed and simulated the potential utility of the NAFLD polygenic risk score, which could be conceptually very advantageous not only for early disease detection but also for implementing actionable measures. Incomplete knowledge of the druggable NAFLD genome severely impedes the drug discovery process and limits the likelihood of identifying robust and safe drug candidates. Thus, we close this article with some insights into emerging disciplines, such as chemical genetics, that may accelerate accurate identification of the druggable NAFLD genome/proteome.

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Original Article

Hepatic neoplasm

Inhibition of PI3K/Akt signaling suppresses epithelial-to-mesenchymal transition in hepatocellular carcinoma through the Snail/GSK-3/beta-catenin pathway: Seulki Lee, Eun Ji Choi, Eun Ju Cho, Yun Bin Lee, Jeong-Hoon Lee, Su Jong Yu, Jung-Hwan Yoon, Yoon Jun Kim; Clin Mol Hepatol 2020;26(4):529-539.
Published online August 24, 2020; DOI: https://doi.org/10.3350/cmh.2019.0056n

Abstract
PDF

Background/Aims
Patients with advanced hepatocellular carcinoma (HCC) have a poor prognosis due to the lack of effective systemic therapies. Epithelial-to-mesenchymal transition (EMT) is a pivotal event in tumor progression, during which cancer cells acquire invasive properties. In this study, we investigated the effects of phosphatidylinositol 3-kinase (PI3K) inhibitors, including LY294002 and idelalisib, on the EMT features of HCC cells in vitro.
Methods
Human HCC cell lines, including Huh-BAT and HepG2, were used in this study. Cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, and cell cycle distributions were evaluated using a flow cytometer by propidium iodide staining. Immunofluorescence staining, quantitative real-time polymerase chain reaction, and immunoblotting were performed to detect EMT-associated changes.
Results
PI3K inhibitors suppressed the proliferation and invasion of HCC cells and deregulated the expression of EMT markers, as indicated by increased expression of E-cadherin, an epithelial marker, and decreased expression of N-cadherin, a mesenchymal marker, and Snail, a transcription factor implicated in EMT regulation. Furthermore, LY294002 and idelalisib inhibited the phosphorylation of GSK-3β and induced the nuclear translocation of GSK-3β, which corresponded to the downregulation of Snail and β-catenin expressions in Huh-BAT and HepG2 cells.
Conclusions
The inhibition of PI3K/Akt signaling decreases Snail expression by enhancing the nuclear translocation of GSK-3β, which suppresses EMT in HCC cells, suggesting the potential clinical application of PI3K inhibitors for HCC treatment.

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Review

Acute liver injury and Acute liver failure

The fibrogenic process and the unleashing of acute-on-chronic liver failure: Guillermo Nahúm López-Sánchez, Mayra Dóminguez-Pérez, Misael Uribe, Natalia Nuño-Lámbarri; Clin Mol Hepatol 2020;26(1):7-15.
Published online June 14, 2019; DOI: https://doi.org/10.3350/cmh.2019.0011

Abstract
PDF

Acute-on-chronic liver failure (ACLF) is a life-threatening condition characterized by a rapid deterioration of previously well-compensated chronic liver diseases. One of the main obstacles in ACLF is the lack of knowledge of the pathogenesis and specific broad-spectrum treatments. An excessive systemic inflammatory response has been proposed to explain the pathogenesis of ACLF; this hypothesis involves stellate cells, which are implicated in many liver homeostatic functions that include vitamin A storage, regulation of sinusoidal blood flow, local inflammation, maintenance of the hepatocyte phenotype and extracellular matrix remodeling. However, when there is damage to the liver, these cells are the main target of the inflammatory stimulus, as a result, the secretion of the extracellular matrix is altered. Activated hepatic stellate cells raise the survival of neutrophils by the stimulation of granulocytes colonies and macrophages, which exacerbates liver inflammation and promotes damage to hepatocytes. Elevation of pathogen-associated molecular patterns is related to liver damage by different pathophysiological mechanisms of decompensation, showing ballooning degeneration and cell death with a predominance of cholestatic infection. Moreover, patients with ACLF present a marked elevation of C-reactive protein together with an elevation of the leukocyte count. Chronic liver disease is a complex pathological state with a heterogeneous pathophysiology in which genetic factors of the host and external triggers interact and culminate in hepatic insufficiency. The better understanding of such interactions should lead to a better comprehension of the disease and to the discovery of new treatment targets that will make acute decompensations preventable and even decrease mortality.

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DibyaLochan Praharaj, Bipadabhanjan Mallick, Preetam Nath, AnilC Anand
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Original Articles

Steatotic liver disease

Effects of different exercise modalities on novel hepatic steatosis indices in overweight women with type 2 diabetes: Ebrahim Banitalebi, Mohammad Faramarzi, Samira Nasiri, Majid Mardaniyan, Vahid Rabiee; Clin Mol Hepatol 2019;25(3):294-304.
Published online May 30, 2019; DOI: https://doi.org/10.3350/cmh.2018.0086

Abstract
PDF

Background/Aims
Fatty liver is a clinical and pathologic condition in individuals with type 2 diabetes (T2D). The purpose of this study is to examine the effects of different exercise modalities on non-alcoholic fatty liver indices (fatty liver index [FLI], lipid accumulation product [LAP], hepatic steatosis index [HSI], and Framingham Steatosis Index [FSI]) in women with T2D.
Methods
Fifty-two women with T2D and a mean age of 55.07±5.92 yrs, body mass index (BMI) 28.94±4.09 kg/m2 , and hemoglobin A1c (HbA1c) 9.41±0.82% were randomized to a sprint interval training (SIT) (n=17), combined aerobic and resistance (A+R) training (n=17), or control group (n=18) for 10 weeks. Two-way repeated analysis of variance (ANOVA) was used to find differences between groups and the effects of time and Time×Group interactions after 10 weeks on non-alcoholic fatty liver indices. After this, ANOVA models were constructed to determine the effects of group allocation and change in non-alcoholic fatty liver indices.
Results
There were significant time interactions for FLI (P<0.001), HSI (P<0.001), and LAP (P<0.001). Also, there were significant Time×Group interactions for fasting blood glucose (P=0.034), and HbA1c (P=0.006).
Conclusions
Results highlight that exercise training, independent of mode of training, is an effective strategy to improve some indices related to hepatic steatosis and blood glucose profiles in women with T2D.

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Effects of cyclic yoga on selected metabolic and hepatic parameters in diabetic women with fatty liver diseases: A clinical trial
Zahra Bayat, Seyedeh Soolmaz Mahdioun, Houshang Nemati, Fatemeh Rezvan Madani, Mehrali Rahimi, Hanieh Dehghan, Rozita Naseri, Seyed Mehdi Goosheh
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Effects of high-intensity interval training on cardiorespiratory fitness and metabolic outcomes in type 2 diabetes: A systematic review and meta-analysis
João Paulo BC Vieira, Vitor Oliveira Carvalho, Luan AC Aguiar, Neil A Smart, Camila Nascimento Monteiro, Mayra Heloise Weege, Rafaella PG da Silva, Bruno N Rangel, Mansueto Gomes-Neto
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Effects of resistance, endurance, and combined exercise training on body composition, glycemic control, and serum albumin in women with type 2 diabetes: A randomized controlled study
Sajjad Ramezani, Reza Farzizadeh, Farnaz Seifi – Asgshahr
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Ebaa Al Ozairi, Mohammad Irshad, Jumana Alkandari, Etab Taghadom, Anisha Varghese, Dherar Alroudhan, Nasser Alqattan, Stuart R. Gray
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Frontiers in Endocrinology.2024;[Epub] CrossRef
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Amjad Abdul Hamid Almajed
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Andressa Karoline Pinto de Lima Ribeiro, Josilayne Patrícia Ramos Carvalho, Natáli Valim Oliver Bento-Torres
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Fatiha Nassir
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Christine L Freer, Elena S George, Sze-Yen Tan, Gavin Abbott, David W Dunstan, Robin M Daly
BMJ Open Diabetes Research & Care.2022; 10(5): e002950. CrossRef
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International Journal of Environmental Research and Public Health.2022; 19(22): 14928. CrossRef
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Hye Won Lee, Jae Seung Lee, Beom Kyung Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Seung Up Kim
Journal of Diabetes and its Complications.2021; 35(1): 107747. CrossRef
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Ho Soo Chun, Jae Seung Lee, Hye Won Lee, Beom Kyung Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn, Yong‐Ho Lee, Young Dae Kim, Seung Up Kim
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Kavita Garg, Trenton Reinicke, Satish K. Garg
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Viral hepatitis

An integrated analysis of elbasvir/grazoprevir in Korean patients with hepatitis C virus genotype 1b infection: Youn Jae Lee, Jeong Heo, Do Young Kim, Woo Jin Chung, Won Young Tak, Yoon Jun Kim, Seung Woon Paik, Eungeol Sim, Susila Kulasingam, Rohit Talwani, Barbara Haber, Peggy Hwang; Clin Mol Hepatol 2019;25(4):400-407.
Published online May 28, 2019; DOI: https://doi.org/10.3350/cmh.2019.0006

Abstract
PDF

Background/Aims
In the Republic of Korea, an estimated 231,000 individuals have chronic hepatitis C virus (HCV) infection. The aim of the present analysis was to evaluate the safety and efficacy of elbasvir/grazoprevir (EBR/GZR) administered for 12 weeks in Korean patients who were enrolled in international clinical trial phase 3 studies.
Methods
This was a retrospective, integrated analysis of data from patients with HCV genotype (GT) 1b infection enrolled at Korean study sites in four EBR/GZR phase 3 clinical trials. Patients were treatment-naive or had previously failed interferon-based HCV therapy, and included those with human immunodeficiency virus coinfection or ChildPugh class A cirrhosis. All patients received EBR 50 mg/GZR 100 mg once daily for 12 weeks. The primary endpoint was sustained virologic response at 12 weeks after completion of therapy (SVR12, HCV RNA <15 IU/mL).
Results
SVR12 was achieved by 73 of 74 (98.6%) patients. No patients had virologic failure and one discontinued from the study after withdrawing consent. SVR12 rates were uniformly high across all patient subgroups. A total of 16 patients had nonstructural protein 5A resistance-associated substitutions at baseline (16/73, 22%), all of whom achieved SVR12. Adverse events (AEs) reported in >5% of patients were fatigue (6.8%), upper respiratory tract infection (5.4%), headache (5.4%), and nausea (5.4%). Thirteen patients (17.6%) reported drug-related AEs, two serious AEs occurred, and two patients discontinued treatment owing to an AEs.
Conclusions
In this retrospective analysis, EBR/GZR administered for 12 weeks was well-tolerated and highly effective in Korean patients with HCV GT1b infection.

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Young Eun Chon, Aejeong Jo, Eileen L. Yoon, Jonghyun Lee, Ho Gyun Shin, Min Jung Ko, Dae Won Jun
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Jieun Lee, Sang Bong Ahn, Sun Young Yim, Jihyun An, Dae Won Jun, Min Jung Ko, Dong Ah Park, Jeong‐Ju Yoo
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Hepatic neoplasm

A survey on transarterial chemoembolization refractoriness and a real-world treatment pattern for hepatocellular carcinoma in Korea: Jae Seung Lee, Beom Kyung Kim, Seung Up Kim, Jun Yong Park, Sang Hoon Ahn, Jin Sil Seong, Kwang-Hyub Han, Do Young Kim; Clin Mol Hepatol 2020;26(1):24-32.
Published online May 20, 2019; DOI: https://doi.org/10.3350/cmh.2018.0065

Background/Aims
Transarterial chemoembolization (TACE) is a standard treatment for intermediate-stage hepatocellular carcinoma (HCC), but there is much controversy about TACE refractoriness. The aim of this study was to identify trends in the actual clinical application of TACE and recognition of TACE refractoriness by Korean experts.
Methods
In total, 17 questionnaires on TACE refractoriness were administered to 161 clinicians via an online survey. Multiple answers were allowed for some questions.
Results
Most clinicians agreed that there is a need for standardization of TACE application through specific scoring systems (n=124, 77.0%). TACE refractoriness was predominantly expected by participants when recurrences were detected within 1 month (n=70, 43.5%), there were 4 to 6 tumors (n=77, 47.8%), the maximal tumor size was 3–5 cm (n=49, 30.4%), and when there was insufficient tumor necrosis despite TACE being repeated more than three times (n=78, 48.4%). Overall, sorafenib therapy (n=137) and radiotherapy (n=114) were preferred when repeated TACE was considered ineffective.
Conclusions
Treatment of HCC is often based on the clinical judgment of clinicians because of the heterogeneity among individuals. Experts need to continue discussions on the standardization and sub-classification of HCC treatment guidelines in Korea.

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Review

Viral hepatitis

Development and surveillance of hepatocellular carcinoma in patients with sustained virologic response after antiviral therapy for chronic hepatitis C: Seong Kyun Na, Byung-Cheol Song; Clin Mol Hepatol 2019;25(3):234-244.
Published online January 21, 2019; DOI: https://doi.org/10.3350/cmh.2018.0108

Abstract
PDF

Hepatitis C virus (HCV) infection is a major risk factor for liver cirrhosis and hepatocellular carcinoma (HCC), and is a leading cause of liver-related deaths worldwide. Recently available direct-acting antiviral agent is very safe and highly effective (>95% sustained virologic response, SVR) against all genotypes of HCV. Achievement of SVR has been associated with a significant reduction of hepatic decompensation, development of HCC, and liver-related mortality. However, HCC risk is not eliminated even after SVR. The annual incidences of HCC in advanced fibrosis or cirrhosis have been estimated to be up to 2.5–4.5% even in patients with SVR. Therefore, surveillance for HCC is recommended in this high-risk patients. In this review, we will describe the clinical outcomes and the risk of HCC in patients with SVR and suggest who should receive surveillance for HCC.

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