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"Metabolic dysfunction-associated steatotic liver disease"

Reply to Correspondence

Reply to correspondence on “Aspirin and HCC risk in MASLD: Nationwide cohort study with genetic risk analysis”
Yang-Hyun Baek
Received January 15, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0068    [Accepted]
  • 185 View
  • 12 Download

Editorial

Aspirin for Hepatocellular Carcinoma Prevention in MASLD: How Far Are We Ready to Proceed? : Editorial on “Aspirin and HCC risk in MASLD: Nationwide cohort study with genetic risk analysis”
Yang-Hyun Baek
Received December 29, 2025  Accepted January 5, 2026  Published online January 9, 2026  
DOI: https://doi.org/10.3350/cmh.2025.1482    [Accepted]
  • 414 View
  • 35 Download

Original Articles

Normal-weight MASLD: reclassification, characteristics, and adverse liver outcomes across diverse populations
Sherlot Juan Song, Eileen Laureal Yoon, Vincent Wai-Sun Wong, Ae Jeong Jo, Grace Lai-Hung Wong, Jimmy Che-To Lai, Dae Won Jun, Terry Cheuk-Fung Yip
Received July 28, 2025  Accepted December 9, 2025  Published online December 12, 2025  
DOI: https://doi.org/10.3350/cmh.2025.0851    [Accepted]
Background & Aims
Previous studies have identified a substantial degree of agreement between the non-alcoholic fatty liver disease (NAFLD) and metabolic dysfunction-associated steatotic liver disease (MASLD) populations, but the same notion may not apply to normal-weight patients with a lower cardiometabolic risk burden. This study aims to investigate the CMRF distributions between normal-weight and overweight/obese MASLD, the agreement between historical NAFLD and MASLD, and to compare the risk of liver-related events (LREs) and all-cause mortality in normal-weight versus overweight or obese MASLD.
Methods
This study included participants with steatotic liver disease (SLD) from five cohorts in Hong Kong, South Korea, and the United States. Participants were recruited from settings including both hospitals and communities. Individuals were classified into normal-weight and overweight/obese groups.
Result
s: This study included 33,793 participants with SLD from five cohorts, of whom 20,893 and 20,701 patients met the diagnosis of NAFLD and MASLD, respectively. Normal-weight patients with NAFLD demonstrated a lower CMRF distribution compared to those with overweight/obese NAFLD. In the community-based cohorts, the proportions of 0 CMRF ranged from 9.0-26.7% among normal-weight NAFLD, representing the discrepancy between MASLD and NAFLD definitions. Compared with the overweight/obese MASLD, the normal-weight MASLD had increased all-cause mortality (normal-weight vs. overweight/obese, 23.44 and 13.80 per 1000 person-years; p<0.001) but not LREs (2.81 and 2.59 per 1000 person-years; p=0.54) in the HK CDARS cohort.
Conclusions
Normal-weight individuals with NAFLD demonstrated a lower distribution of CMRFs, resulting in the incomplete agreement between historical NAFLD and MASLD.
Ethical Compliance
For all involved cohorts, the study protocols conformed to the ethical guidelines of the 1975 Declaration of Helsinki and were approved by the appropriate clinical research ethics committee and/or institutional review board, which provided either written consent or a waiver of informed consent.

Citations

Citations to this article as recorded by  Crossref logo
  • Challenges in defining MASLD in lean individuals: the impact of the Fatty Liver Index on phenotypic characterisation
    Sherlot Juan Song, Yiwei Liu, Vincent Wai-Sun Wong, Terry Cheuk-Fung Yip
    Gut.2026; : gutjnl-2026-338216.     CrossRef
  • 1,147 View
  • 151 Download
  • Crossref
Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes video
Le Bich Hang Pham, Taeeung Kim, Seoyoung Kim, Yun Seok Kim, Jiyeon Kim, Kyeongseon Kim, Hyeonwoo Lim, Wan Seob Shim, Byoungmo Kim, So-Yeol Yoo, Jae-Young Lee, Murim Choi, Won Kim, Keon Wook Kang, Jeeyeon Lee
Clin Mol Hepatol 2026;32(1):318-338.
Published online November 17, 2025
DOI: https://doi.org/10.3350/cmh.2025.0779
Background/Aims
Ferroptosis, recently emerged as a new cell death modality characterized by iron-dependent peroxidation of lipids, has been explored in various diseases. However, detection of ferroptosis, particularly in chronic liver disease models, is hampered by the lack of universal ferroptosis markers and limited number of fluorescence sensors for in vivo ferroptosis.
Methods
In this study, we developed TTM-4 as a highly sensitive near-infrared (NIR) fluorescent probe to detect ferroptosis.
Result
s: TTM-4 exhibited turn-on fluorescence upon viscosity change, enabling visualization of lipid peroxidation (LPO) in ferroptotic hepatocytes and liver tissue samples with greater sensitivity than BODIPY 581/591 C11. Timelapse live-cell imaging of erastin-treated cells revealed real-time LPO dynamics involving cytosolic lipid droplets (cLDs), endoplasmic reticulum, and nuclear LDs in a chronological order. Further gene expression analysis of 216 liver tissue samples from the NCBI GEO database showed a significant increase in CIDEC concurrent with TTM-4 fluorescence during progression to metabolic dysfunction-associated steatotic hepatitis (MASH). TTM-4, with its low toxicity and turn-on NIR emission during ferroptosis, also enabled in vivo visualization of ferroptosis in liver injury and metabolic dysfunction-associated steatotic liver disease (MASLD) models.
Conclusions
Our findings suggest that TTM-4 enables monitoring of ferroptosis in MASLD and would aid in early MASH diagnosis.
  • 1,655 View
  • 179 Download
Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement
Joseph Rabbat, Boyu Yang, Hye Won Lee, Huapeng Lin, Emmanuel Tsochatzis, Salvatore Petta, Elisabetta Bugianesi, Masato Yoneda, Ming-Hua Zheng, Hannes Hagström, Jérôme Boursier, José Luis Calleja, George Boon-Bee Goh, Wah-Kheong Chan, Rocio Gallego-Durán, Arun J. Sanyal, Victor de Lédinghen, Philip N Newsome, Jian-Gao Fan, Laurent Castéra, Michelle Lai, Céline Fournier-Poizat, Grace Lai-Hung Wong, Mirko Zoncape, Grazia Pennisi, Angelo Armandi, Atsushi Nakajima, Wen-Yue Liu, Ying Shang, Marc de Saint-Loup, Elba Llop, Kevin Kim Jun Teh, Carmen Lara-Romero, Amon Asgharpour, Sara Mahgoub, Mandy Sau-Wai Chan, Clemence M Canivet, Manuel Romero-Gomez, Vincent Wai-Sun Wong, Seung Up Kim, Terry Cheuk-Fung Yip
Clin Mol Hepatol 2026;32(1):289-304.
Published online November 11, 2025
DOI: https://doi.org/10.3350/cmh.2025.0888
Background/Aims
Current guidelines recommend a 2-step approach for identifying advanced fibrosis in metabolic dysfunction-associated steatotic liver disease (MASLD), using Fibrosis-4 index (FIB-4) followed by liver stiffness measurement (LSM) via vibration-controlled transient elastography (VCTE). However, some patients may exhibit discordant results. This study evaluates the histological severity and outcomes in patients with discordant FIB-4 and LSM results.
Methods
This secondary analysis of the VCTE-Prognosis study included 12,950 patients evaluated for MASLD at 16 tertiary centers, of whom 2,915 underwent liver biopsy. Patients were categorized into four groups based on established FIB-4 (1.3) and LSM (8 kPa) cutoffs.
Result
s: F3–F4 fibrosis was observed in 6.4%, 13.7%, 30.6%, and 62.4% in low-FIB-4-low-LSM (n=6,403), high-FIB-4-low-LSM (n=3,017), low-FIB-4-high-LSM (n=1,363), and high-FIB-4-high-LSM (n=2,167) groups, respectively. During a median follow-up of 47.4 months, 248 patients experienced hepatic decompensation, hepatocellular carcinoma, liver transplantation, or liver-related death. The incidence rates of liver-related events (LREs) were 0.67, 1.19, 2.58, and 21.30 per 1,000 person-years, respectively. Compared to low-FIB-4-low-LSM patients, those with low-FIB-4-high-LSM (adjusted subdistribution hazard ratio [aSHR] 4.12) and high-FIB-4-high-LSM (aSHR 21.38) had a significantly higher risk of LREs, while high-FIB-4-low-LSM patients did not. Similar findings were observed when hepatic decompensation and hepatocellular carcinoma were analyzed separately.
Conclusions
Approximately 30% of patients in tertiary centers exhibit discordant FIB-4 and LSM results, with LSM more likely reflecting true severity. While some patients with discordant results may have advanced fibrosis, the overall incidence of LREs remains low.
  • 2,539 View
  • 298 Download
Evaluating treatment response thresholds for cost-effective treatment in metabolic dysfunction-associated steatotic liver disease
Eileen L. Yoon, Jeong-Yeon Cho, Huiyul Park, Mimi Kim, Ji-Hyeon Park, Hye-Lin Kim, Dae Won Jun
Clin Mol Hepatol 2026;32(1):276-288.
Published online November 3, 2025
DOI: https://doi.org/10.3350/cmh.2025.0796
Background/Aims
The first metabolic dysfunction-associated steatotic liver disease (MASLD) drug was approved with an unsatisfactorily small effect size. This study aimed to determine key factors impacting the cost-effectiveness of a new hypothetical MASLD drug as well as its treatment efficacy.
Methods
A Markov model reflecting the natural history of MASLD was developed, incorporating fibrosis progression, cardiovascular disease risk, and mortality. Treatment effect of drug X (with $20,000 of annual cost) was assumed to achieve a ≥1 stage fibrosis regression, with a 25% gap of effect size in regression rate over non-treatment in the first year. The incremental cost-effectiveness ratio (ICER) over a 20-year horizon was estimated. And sensitivity analyses were conducted to explore uncertainty and identify influential factors.
Result
s: In the base case analysis, drug X provided an incremental gain of 1.32 quality-adjusted life years (QALYs) and 1.20 life years compared to the non-treatment, with an ICER of $68,010/QALY–below the $100,000/QALY willingnessto- pay threshold, indicating that drug X treatment is cost-effective. Two-way sensitivity analysis further highlighted that the drug should achieve at least a 15% initial regression gap and maintain a minimum 3% sustained durability gap to remain cost-effective. In addition baseline fibrosis stage distribution also acted as an influencing factor.
Conclusions
Long-term sustained durability of the hypothetical drug, patient distribution based on baseline fibrosis stage, as well as initial treatment response rate are key factors that influence the cost-effectiveness of new MASLD drugs.
  • 1,083 View
  • 111 Download
Bacteroides eggerthii ameliorates metabolic dysfunction-associated steatotic liver disease through host–microbe signaling and highlights 2-hydroxyisocaproate as a potential effector
Jiyi Choi, Moon Gyeong Yoon, Se Ha Jang, Geum Ok Baek, Hyun Sun Jung, Na-Rae Lee, Choong Hwan Lee, Ji Eun Han, Jae Youn Cheong, Jung Woo Eun, Soon Sun Kim
Clin Mol Hepatol 2026;32(1):239-257.
Published online October 27, 2025
DOI: https://doi.org/10.3350/cmh.2025.0475
Background/Aims
Gut microbiome plays a pivotal role in metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis, yet, associated functional mechanisms and host responses of specific microbial species remain insufficiently characterized. This study investigated the Bacteroides eggerthii therapeutic effects on MASLD by integrating multi-omics analysis and experimental validation in a Western diet (WD)-induced mouse model.
Methods
Candidate strains were identified using 16S rRNA gene sequencing of fecal samples from individuals with and without MASLD or obesity. B. eggerthii, a species significantly depleted in both groups, was selected for functional evaluation. Male C57BL/6J mice were fed a WD or WD supplemented with B. eggerthii (WD+B) for 12 weeks. Liver histology, serum biochemistry, fecal microbiome and metabolome profiling, and hepatic and intestinal transcriptomic analyses were performed. Anti-steatotic effects of B. eggerthii–derived metabolites were validated in vitro.
Result
s: Bacteroides eggerthii supplementation significantly improved liver weight, inflammation, fibrosis, and steatosis in WD+B group compared to WD alone. PICRUSt-based LEfSe analysis revealed choloylglycine hydrolase activity enrichment in gut microbiota, and strain-specific qPCR confirmed colonization in mouse colon. Integrated transcriptomic analyses revealed lipid and bile acid signaling pathway restoration, including CD36, FXR, and FGF15. Untargeted metabolomics identified elevated 2-hydroxyisocaproic acid (HICA) as a strain-derived metabolite in feces and B. eggerthii culture supernatants. In vitro, HICA significantly reduced lipid accumulation in free fatty acid-induced steatosis models.
Conclusions
Bacteroides eggerthii ameliorates MASLD via gut-liver axis modulation, including bile acid metabolism and hepatic lipid signaling. These underscore its therapeutic potential and highlight HICA as a novel microbiome-derived metabolite with anti-steatotic activity.
  • 2,426 View
  • 391 Download

Correspondences

Correspondence to the editorial “ASB3 degrades the gateway to β-oxidation: on Hepatocytic ASB3 deficiency alleviates MASLD by decreasing ubiquitin-mediated CPT1A”
Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan
Received September 25, 2025  Accepted September 27, 2025  Published online September 29, 2025  
DOI: https://doi.org/10.3350/cmh.2025.1100    [Accepted]
  • 942 View
  • 56 Download
Correspondence to the editorial on “Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease (CHM-2025-1013)”
Yuli Lin, Dongqin Yang, Zhihao Wu, Ming Guan, Chunhua Song
Received September 23, 2025  Accepted September 27, 2025  Published online September 29, 2025  
DOI: https://doi.org/10.3350/cmh.2025.1086    [Accepted]
  • 799 View
  • 35 Download

Editorial

Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease
Yueying Yang, Ying Yang, Yan Lu
Received September 8, 2025  Accepted September 8, 2025  Published online September 15, 2025  
DOI: https://doi.org/10.3350/cmh.2025.1013    [Accepted]
  • 1,267 View
  • 58 Download

Letter to the Editor

Comment on “High Steatosis-Associated Fibrosis Estimator Scores Predict Hepatocellular Carcinoma in Viral and Non-Viral Hepatitis and Metabolic Dysfunction-Associated Steatotic Liver Disease”
Prajnasini Satapathy, Rachana Mehta, Ranjana Sah
Received August 2, 2025  Accepted August 6, 2025  Published online August 8, 2025  
DOI: https://doi.org/10.3350/cmh.2025.0875    [Accepted]
  • 2,821 View
  • 23 Download

Original Article

Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A
Yuli Lin, Wulei Hou, Mengxiao Ge, Zhihao Wu, Linlin Huang, Haoye Liu, Wenli Zhang, Xiyu Deng, Lanxin Wang, Ming Guan, Chunhua Song, Zuoyun Wang, Dongqin Yang
Clin Mol Hepatol 2025;31(4):1333-1354.
Published online August 8, 2025
DOI: https://doi.org/10.3350/cmh.2024.1041
Background/Aims
Excessive lipid accumulation in hepatocytes is a critical cause of metabolic dysfunction-associated steatotic liver disease (MASLD) progression. Ankyrin repeat and SOCS box protein 3 (ASB3) is an E3 ubiquitin ligase that mediates diverse disease processes; however, the direct substrates of ASB3 in lipid metabolism and its role in MASLD remain unexplored.
Methods
We generated ASB3 knockout mice fed a high-fat diet to induce MASLD. Oxygen consumption and fatty acid oxidation (FAO) were used to assess lipid metabolism. LC-MS/MS and IP were used to verify the ASB3 target protein. Correlation analysis was conducted on the cohort of MASLD patients vs. the control group.
Result
s: Loss of the ASB3 E3 ubiquitin ligase in hepatocytes strengthens mitochondrial FAO, thereby influencing energy consumption to decrease triglyceride storage and lipid accumulation. Quantitative lysine ubiquitination proteomics revealed that ASB3 directly mediated the ubiquitin levels at two sites (K180 and K639) in carnitine palmitoyl transferase 1A (CPT1A), a rate-limiting enzyme of FAO, to induce CPT1A degradation. Moreover, both constitutive and hepatocyte-specific ASB3 knockout enhance FAO and delay lipid accumulation, liver steatosis, and MASLD progression in a CPT1A-dependent manner. Hepatic ASB3 deficiency also delays fibrosis in MASLD. Analysis of public databases and liver tissue samples from MASLD patients revealed that ASB3 was highly expressed in MASLD patients and was negatively correlated with CPT1A.
Conclusions
Our study reveals the key roles of ASB3 in the development of MASLD and suggests a novel therapeutic potential for MASLD.
  • 4,745 View
  • 492 Download

Editorials

GLP-1RA may open a new era for MASLD treatment
Ye Feng, Chengfu Xu
Received June 12, 2025  Accepted June 19, 2025  Published online June 24, 2025  
DOI: https://doi.org/10.3350/cmh.2025.0628    [Accepted]
  • 2,217 View
  • 77 Download
Risk stratification of metabolic dysfunction-associated steatotic liver disease: The KASL pathway: Editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease”
May Xuan Goh, Xin En Goh, Jarell Jie-Rae Tan, Vincent L Chen, Yu Jun Wong
Clin Mol Hepatol 2026;32(1):429-431.
Published online April 28, 2025
DOI: https://doi.org/10.3350/cmh.2025.0420

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease”
    Hye Won Lee, Seung Up Kim
    Clinical and Molecular Hepatology.2026; 32(1): e87.     CrossRef
  • 5,293 View
  • 41 Download
  • Crossref

Original Article

Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study
Xianhua Mao, Xinrong Zhang, Rongtao Lai, Ka-Shing Cheung, Man-Fung Yuen, Ramsey Cheung, Wai-Kay Seto, Mindie H. Nguyen
Clin Mol Hepatol 2025;31(3):1084-1099.
Published online April 23, 2025
DOI: https://doi.org/10.3350/cmh.2024.1096
Background/Aims
Information about the association of glucagon-like peptide-1 receptor (GLP-1RA) with liver and non-liver complications is insufficient in patients with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD). We conducted a target trial emulation study to evaluate whether GLP-1RA decreases the risk of liver and non-liver outcomes.
Methods
Patients with T2D and MASLD initiating GLP-1RA or dipeptidyl peptidase-4 inhibitor (DPP-4i) were included from 2013 to 2022 in Merative™ Marketscan® Research Databases. Primary outcomes included incidences of (1) hepatocellular carcinoma (HCC) and cirrhosis, and (2) cardiovascular disease (CVD), chronic kidney disease (CKD), and non-liver cancer. Inverse probability of treatment weighting was applied to balance baseline characteristics and Cox regression models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).
Result
s: In the intention-to-treat design, GLP-1RA, compared with DPP-4i, had a significantly lower incidence (per 1,000 person-years) of HCC (0.8 vs. 1.7; HR 0.53, 95% CI 0.39–0.71), of cirrhosis (29.3 vs. 32.9; HR 0.91, 95% CI 0.86–0.96), of CVD (57.2 vs. 73.9; HR 0.90, 95% CI 0.86–0.95), of CKD (4.5 vs. 6.8; HR 0.73, 95% CI 0.64–0.84), and of non-liver cancer (16.9 vs. 22.9; HR 0.82, 95% CI 0.77–0.89). In the per-protocol design, significant inverse associations for these study outcomes still were observed, with HR 0.60–0.77.
Conclusions
In this emulated target trial of nationwide patients with T2D and MASLD, GLP-1RA use, when compared with DPP-4i, was associated with a significantly lower risk of liver and non-liver complications.

Citations

Citations to this article as recorded by  Crossref logo
  • Tirzepatide versus SGLT2 inhibitors for MASLD: a multi-institutional propensity score-matched cohort study
    Jheng-Yan Wu, Yu-Min Lin, Wan-Hsuan Hsu, Ting-Hui Liu, Ya-Wen Tsai, Po-Yu Huang, Min-Hsiang Chuang, Tsung Yu, Chih-Cheng Lai
    Hepatology International.2026;[Epub]     CrossRef
  • Evaluating causal protective effect of dual GLP-1R/GIPR agonists on MASLD: A Mendelian randomization and colocalization study
    Yangke Cai, Siyuan Xie, Liyi Xu, Jiamin Chen, Jianting Cai
    European Journal of Pharmacology.2025; 1005: 178088.     CrossRef
  • Impaired Thyroid Hormone Sensitivity is Associated with Increased Risk of Liver Fibrosis in Euthyroid Population: A Cross-Sectional Analysis of NHANES
    Xingyu Yao, Kaiwen Xiao, Hein Ko Oo
    Hormone and Metabolic Research.2025; 57(09): 511.     CrossRef
  • 12,381 View
  • 287 Download
  • 4 Web of Science
  • Crossref

Editorial

Metabolic health in antiviral era of chronic hepatitis B: Editorial on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues”
Shang-Chin Huang, Jia-Horng Kao
Clin Mol Hepatol 2026;32(1):423-425.
Published online April 11, 2025
DOI: https://doi.org/10.3350/cmh.2025.0369

Citations

Citations to this article as recorded by  Crossref logo
  • Advancing metabolic risk profiling in chronic hepatitis B: Reply to correspondence on “Metabolic health in antiviral era of chronic hepatitis B”
    Shang-Chin Huang, Jia-Horng Kao
    Clinical and Molecular Hepatology.2026; 32(1): e117.     CrossRef
  • Correspondence to editorial 1 on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues”
    Rui Huang, Mindie H. Nguyen
    Clinical and Molecular Hepatology.2026; 32(1): e83.     CrossRef
  • 4,420 View
  • 43 Download
  • Crossref

Review

Emerging therapies and real-world application of metabolic dysfunction-associated steatotic liver disease treatment
Hee Yeon Kim, Mary E. Rinella
Clin Mol Hepatol 2025;31(3):753-770.
Published online April 2, 2025
DOI: https://doi.org/10.3350/cmh.2025.0083
Metabolic dysfunction-associated steatotic liver disease, formerly referred to as non-alcoholic fatty liver disease, is the most common liver disease in Western countries and has emerged as the leading indication for liver transplantation. Metabolic dysfunction-associated steatohepatitis (MASH), a more advanced stage, carries a high risk of progression to liver fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. Until recently, lifestyle intervention remained the mainstay of MASH management, with no pharmacological treatments specifically approved. However, advances in understanding its pathophysiological mechanisms have fueled numerous clinical trials, culminating in the Food and Drug Administration’s (FDA) approval of resmetirom as the first treatment for MASH in 2024. Additionally, many investigational drugs are nearing FDA approval or progressing through late-stage clinical trials. This review examines the current therapeutic landscape, highlights strategies for identifying patients suitable for liver-directed therapies in real-world settings, and discusses the challenges that remain.

Citations

Citations to this article as recorded by  Crossref logo
  • Quzhou-sourced Fructus Aurantii ameliorates MASLD by modulating glycolysis-dependent M1 polarization in hepatic macrophages
    Junbin Yan, Yunmeng Nie, Menglu Ding, Mi Zhou, Tingyuan Li, Sumei Xu, Shuo Zhang
    Phytomedicine.2026; 150: 157572.     CrossRef
  • Stimuli-responsive nanomedicines for hepatic diseases: mechanism, design, recent advances, and clinical translation
    Leyi Wang, Xue Zhang, Yinggang Li, Min Zhao, Gang Xu, Zhenyu Duan, Qiyong Gong, Kui Luo
    Journal of Controlled Release.2026; 390: 114522.     CrossRef
  • Convergent Metabolic Pathways in MASH Therapeutics: An AMPK‐Centric Analysis
    Seungchan Choi, Jin‐Seok Jung, Yie‐sung Seo, Sungmin Song, Jeehye Ham, Hannah Chung, Yousef Ramadan, Kangchan Choi
    Journal of Cellular and Molecular Medicine.2026;[Epub]     CrossRef
  • Steatotic Liver Disease in Older Adults: Clinical Implications and Unmet Needs
    Daniel Clayton-Chubb, William W. Kemp, Ammar Majeed, Peter W. Lange, Jessica A. Fitzpatrick, Karl Vaz, John S. Lubel, Alexander D. Hodge, Joanne Ryan, John J. McNeil, Alice J. Owen, Robyn L. Woods, Stuart K. Roberts
    Nutrients.2025; 17(13): 2189.     CrossRef
  • Tirzepatide in metabolic dysfunction-associated steatotic liver disease and steatohepatitis: a novel star on the horizon?
    Amedeo Lonardo, Ralf Weiskirchen
    Exploration of Drug Science.2025;[Epub]     CrossRef
  • Timosaponin AIII from Anemarrhena asphodeloides binds and inhibits S100A8-mediated neutrophil infiltration and NET formation ameliorates MASH
    Yunfan Bai, Jingxin Ju, Ruishi Xie, Jing Li, Xinyi Zhao, Xiaoxue Fang, Ming Zhu, Xintian Lan, Haoming Luo
    International Immunopharmacology.2025; 166: 115539.     CrossRef
  • Full Active Nanoplatform Restores ROS Homeostasis for Synergistic Therapy of Fatty Liver Disease via Dual Endogenous–Exogenous Pathways
    Ziyi Lin, Peng Xu, Yuehai Xu, Yixin Zheng, Huimin Li, Zixin Chen, Zhe Wang, Shaochen Song, Yuhao Liu, Zhao Yang, Ju Cui, Heyun Shen
    ACS Applied Materials & Interfaces.2025;[Epub]     CrossRef
  • From mechanisms to management: Early detection and improved treatment of MASLD and its related hepatocellular carcinoma
    Dingwu Li, Xiang Zhang
    Hepatology Communications.2025;[Epub]     CrossRef
  • Editorial: Combination Therapies for MASH: A Step Forward or More Complexity?
    Xiao‐Dong Zhou, Yusuf Yilmaz, Mazen Noureddin, Hung N. Luu, Ming‐Hua Zheng
    Alimentary Pharmacology & Therapeutics.2025;[Epub]     CrossRef
  • Combination therapies for metabolic dysfunction-associated steatohepatitis: challenges and opportunities
    Xiao-Dong Zhou, Qiong-Yue Fan, Christopher D Byrne, Giovanni Targher, Mark D Muthiah, Daniel Q Huang, Qin-Fen Chen, Mazen Noureddin, Wenhao Li, Vlad Ratziu, Rohit Loomba, Sven M Francque, Arun J Sanyal, Ming-Hua Zheng
    Gut.2025; : gutjnl-2025-337431.     CrossRef
  • 11,887 View
  • 312 Download
  • 8 Web of Science
  • Crossref

Letter to the Editor

Letter to the editor on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Weixiong Zhu, Xuefan Zeng, Zengxi Yang, Yusheng Cheng, Wence Zhou
Clin Mol Hepatol 2025;31(3):e252-e253.
Published online February 26, 2025
DOI: https://doi.org/10.3350/cmh.2025.0189
  • 8,595 View
  • 77 Download

Editorial

Risk stratification for hepatocellular carcinoma in metabolic dysfunction-associated steatotic liver disease: Editorial on “High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated steatotic liver disease”
Ho Soo Chun, Minjong Lee
Clin Mol Hepatol 2026;32(1):368-370.
Published online February 11, 2025
DOI: https://doi.org/10.3350/cmh.2025.0116
  • 5,835 View
  • 40 Download

Letter to the Editor

What is new in the 2024 Chinese guidelines for fatty liver disease?
Rui-Xu Yang, Vincent Wai-Sun Wong, Jian-Gao Fan
Clin Mol Hepatol 2025;31(3):e239-e246.
Published online January 21, 2025
DOI: https://doi.org/10.3350/cmh.2024.1165
  • 9,878 View
  • 94 Download

Correspondence

Steatotic liver disease

Age serves as the silent architect of FIB-4’s precision in unveiling advanced hepatic fibrosis in MASLD with T2DM: Correspondence to letter to the editor on “Diagnostic accuracy of the fibrosis-4 index for advanced liver fibrosis in nonalcoholic fatty liver disease with type 2 diabetes: a systematic review and meta-analysis”
Ji Won Han, Dae Won Jun
Clin Mol Hepatol 2025;31(2):e152-e154.
Published online December 30, 2024
DOI: https://doi.org/10.3350/cmh.2024.1160

Citations

Citations to this article as recorded by  Crossref logo
  • Non-invasive Risk-based Surveillance Strategy for Hepatocellular Carcinoma in Patients with Metabolic Dysfunction-associated Steatotic Liver Disease
    Ji Won Han
    The Korean Journal of Gastroenterology.2026; 86(1): 62.     CrossRef
  • 6,562 View
  • 43 Download
  • Crossref

Editorial

Steatotic liver disease

A leap in the dark: Bariatric surgery for treatment of metabolic dysfunction-associated steatotic liver disease related cirrhosis: Editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
Jing Zeng, Jian-Gao Fan
Clin Mol Hepatol 2025;31(2):610-614.
Published online December 17, 2024
DOI: https://doi.org/10.3350/cmh.2024.1099

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
    Nicholas A. Rouillard, Linda Henry, Mindie H. Nguyen
    Clinical and Molecular Hepatology.2025; 31(2): e173.     CrossRef
  • Reply to correspondence on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
    Jing Zeng, Jian-Gao Fan
    Clinical and Molecular Hepatology.2025; 31(2): e218.     CrossRef
  • 7,076 View
  • 51 Download
  • 2 Web of Science
  • Crossref

Review

Steatotic liver disease

Microbiome-centered therapies for the management of metabolic dysfunction-associated steatotic liver disease
Huma Saeed, Luis Antonio Díaz, Antonio Gil-Gómez, Jeremy Burton, Jasmohan S. Bajaj, Manuel Romero-Gomez, Marco Arrese, Juan Pablo Arab, Mohammad Qasim Khan
Clin Mol Hepatol 2025;31(Suppl):S94-S111.
Published online November 28, 2024
DOI: https://doi.org/10.3350/cmh.2024.0811
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a significant global health issue, affecting over 30% of the population worldwide due to the rising prevalence of metabolic risk factors such as obesity and type 2 diabetes mellitus. This spectrum of liver disease ranges from isolated steatosis to more severe forms such as steatohepatitis, fibrosis, and cirrhosis. Recent studies highlight the role of gut microbiota in MASLD pathogenesis, showing that dysbiosis significantly impacts metabolic health and the progression of liver disease. This review critically evaluates current microbiome-centered therapies in MASLD management, including prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and emerging therapies such as engineered bacteria and bacteriophage therapy. We explore the scientific rationale, clinical evidence, and potential mechanisms by which these interventions influence MASLD. The gut-liver axis is crucial in MASLD, with notable changes in microbiome composition linked to disease progression. For instance, specific microbial profiles and reduced alpha diversity are associated with MASLD severity. Therapeutic strategies targeting the microbiome could modulate disease progression by improving gut permeability, reducing endotoxin-producing bacteria, and altering bile acid metabolism. Although promising, these therapies require further research to fully understand their mechanisms and optimize their efficacy. This review integrates findings from clinical trials and experimental studies, providing a comprehensive overview of microbiome-centered therapies’ potential in managing MASLD. Future research should focus on personalized strategies, utilizing microbiome features, blood metabolites, and customized dietary interventions to enhance the effectiveness of these therapies.

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Original Article

Steatotic liver disease

Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis
Nicholas A. Rouillard, Scott D. Barnett, Xinrong Zhang, Leslie Kam, Richie Manikat, Ramsey Cheung, Mindie H. Nguyen
Clin Mol Hepatol 2025;31(1):227-239.
Published online November 14, 2024
DOI: https://doi.org/10.3350/cmh.2024.0564
Background/Aims
With the obesity pandemic, metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease and a leading cause of end-stage liver disease and liver-related deaths in the USA. Therefore, we aimed to compare the long-term outcomes of patients with MASLD and cirrhosis with and without bariatric surgery.
Methods
Patients were retrospectively identified from the California Department of Healthcare Access and Information database, 2005 to 2019, for a population-based cohort study. Propensity score matching (PSM) was used to balance background risks between patients with cirrhosis who underwent bariatric surgery and those who did not. Overall, liver-related and non-liver-related mortality were analyzed.
Result
s: Of 91,708 eligible patients with MASLD and cirrhosis, PSM yielded 2,107 patients who underwent bariatric surgery and 8,428 non-bariatric controls. Compared to matched controls, patients who underwent bariatric surgery had lower 5-year overall (24.9% vs. 37.1%; p<0.0001), liver-related (3.3% vs. 14%; p<0.0001), and non-liver-related mortality (22.3% vs. 26.9%; p=0.046). In multivariable analysis, bariatric surgery was associated with decreased overall mortality (adjusted hazard ratio [aHR]=0.63; p<0.0001), liver-related (aHR=0.24; p<0.0001), and non-liverrelated (aHR=0.81; p=0.0026) mortality. However, only laparoscopic surgeries were associated with lower overall mortality (aHR=0.39; p<0.0001) whereas open surgeries were associated with higher overall mortality (aHR=1.24; p=0.022).
Conclusions
Patients with MASLD and cirrhosis who underwent bariatric surgery, specifically laparoscopic approaches, had significantly lower mortality risk than non-surgical counterparts.

Citations

Citations to this article as recorded by  Crossref logo
  • Differential Characteristics and Survival Outcomes of Patients With Cirrhosis According to Underlying Liver Aetiology
    Yu Shi, Nicholas Chien, Ashley Fong, Vy H. Nguyen, Surya Teja Gudapati, Angela Chau, Sally Tran, Linda Henry, Ramsey Cheung, Changqing Zhao, Minjuan Jin, Mindie H. Nguyen
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  • A leap in the dark: Bariatric surgery for treatment of metabolic dysfunction-associated steatotic liver disease related cirrhosis: Editorial on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic live
    Jing Zeng, Jian-Gao Fan
    Clinical and Molecular Hepatology.2025; 31(2): 610.     CrossRef
  • Letter to the editor on “Bariatric surgery reduces long-term mortality in patients with metabolic dysfunction-associated steatotic liver disease and cirrhosis”
    Wei Wang, Yating Xie, Ailei Xu
    Clinical and Molecular Hepatology.2025; 31(2): e143.     CrossRef
  • Advancing precision medicine in metabolic dysfunction-associated steatotic liver disease
    Bryan A. Priego-Parra, Rocío Gallego-Durán, Berenice M. Román-Calleja, José Antonio Velarde-Ruiz Velasco, Manuel Romero-Gómez, Jordi Gracia-Sancho
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    Nicholas A. Rouillard, Linda Henry, Mindie H. Nguyen
    Clinical and Molecular Hepatology.2025; 31(2): e173.     CrossRef
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    Jing Zeng, Jian-Gao Fan
    Clinical and Molecular Hepatology.2025; 31(2): e218.     CrossRef
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    Weixiong Zhu, Xuefan Zeng, Zengxi Yang, Yusheng Cheng, Wence Zhou
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    Yanshan Yi, Li Yang
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    Chi-Kuei Hsu, Po-Yu Huang, Chih-Cheng Lai
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    Pandora Fonseca, Leonardo Pereira, João Gabriel Braga, Giovanna Macanhã Scremin, Luísa de Araujo, Julia Alves, Gabriel de França, Pedro Bregion, Rafael Rego, Maria Farias, Victor Ivano
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    Janna Vanessa Diaz Torres, Vanessa Rocío Villanueva Guerrero, Jennifer Patricia Vargas Gómez, Fredy Javier Pacheco Miranda, Lorena Rocío Orozco Álvarez, Joseph David León Insignares, Marian Mares, Héctor Mario Rodríguez Ortiz, Evelyn Mendoza-Torres
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  • 7,049 View
  • 181 Download
  • 10 Web of Science
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Editorial

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

Citations

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  • 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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    Cell Death & Differentiation.2025;[Epub]     CrossRef
  • 7,437 View
  • 125 Download
  • 3 Web of Science
  • Crossref

Review

Steatotic liver disease

Bioactive metabolites: A clue to the link between MASLD and CKD?
Wen-Ying Chen, Jia-Hui Zhang, Li-Li Chen, Christopher D. Byrne, Giovanni Targher, Liang Luo, Yan Ni, Ming-Hua Zheng, Dan-Qin Sun
Clin Mol Hepatol 2025;31(1):56-73.
Published online October 21, 2024
DOI: https://doi.org/10.3350/cmh.2024.0782
Metabolites produced as intermediaries or end-products of microbial metabolism provide crucial signals for health and diseases, such as metabolic dysfunction-associated steatotic liver disease (MASLD). These metabolites include products of the bacterial metabolism of dietary substrates, modification of host molecules (such as bile acids [BAs], trimethylamine-N-oxide, and short-chain fatty acids), or products directly derived from bacteria. Recent studies have provided new insights into the association between MASLD and the risk of developing chronic kidney disease (CKD). Furthermore, alterations in microbiota composition and metabolite profiles, notably altered BAs, have been described in studies investigating the association between MASLD and the risk of CKD. This narrative review discusses alterations of specific classes of metabolites, BAs, fructose, vitamin D, and microbiota composition that may be implicated in the link between MASLD and CKD.

Citations

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  • Radish Green Extract Attenuates Western Diet-Induced Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease in Mice
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Correspondence

Liver fibrosis, cirrhosis, and portal hypertension

Correspondence to editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: a systematic review and meta-analysis”
Young Eun Chon, Jung Hwan Yu, Seung Up Kim
Clin Mol Hepatol 2025;31(1):e61-e63.
Published online October 15, 2024
DOI: https://doi.org/10.3350/cmh.2024.0878
  • 5,736 View
  • 45 Download

Editorial

Steatotic liver disease

Essential tools for assessing advanced fibrosis in metabolic dysfunction-associated steatotic liver disease: Editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: A systematic review and meta-analysis”
Won Sohn
Clin Mol Hepatol 2025;31(1):277-280.
Published online October 11, 2024
DOI: https://doi.org/10.3350/cmh.2024.0823

Citations

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    Na Tian, Tie Xiao, Tianyi Xia, Hai‐Yang Yuan, Michael D. Shapiro, Gregory Y. H. Lip, Cheng‐Han Fanren, Li‐You Lian, Chen‐Xiao Huang, Yi‐Xuan Wei, Giovanni Targher, Christopher D. Byrne, Cheng‐Lv Hong, Shenghong Ju, Ming‐Hua Zheng
    Alimentary Pharmacology & Therapeutics.2026; 63(1): 70.     CrossRef
  • Correspondence to editorial on “Optimal cut-offs of vibration-controlled transient elastography and magnetic resonance elastography in diagnosing advanced liver fibrosis in patients with nonalcoholic fatty liver disease: a systematic review and meta-analy
    Young Eun Chon, Jung Hwan Yu, Seung Up Kim
    Clinical and Molecular Hepatology.2025; 31(1): e61.     CrossRef
  • Impact of Short-Term Liraglutide Therapy on Non-Invasive Markers of Liver Fibrosis in Patients with MASLD
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    Metabolites.2025; 15(8): 510.     CrossRef
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    World Journal of Hepatology.2025;[Epub]     CrossRef
  • 6,758 View
  • 55 Download
  • 4 Web of Science
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Review

Artificial intelligence, epidemiology, methodology, or others

Roles of X-box binding protein 1 in liver pathogenesis
Jihoon Tak, Yun Seok Kim, Sang Geon Kim
Clin Mol Hepatol 2025;31(1):1-31.
Published online October 2, 2024
DOI: https://doi.org/10.3350/cmh.2024.0441
The prevalence of drug-induced liver injury (DILI) and viral liver infections presents significant challenges in modern healthcare and contributes to considerable morbidity and mortality worldwide. Concurrently, metabolic dysfunctionassociated steatotic liver disease (MASLD) has emerged as a major public health concern, reflecting the increasing rates of obesity and leading to more severe complications such as fibrosis and hepatocellular carcinoma. X-box binding protein 1 (XBP1) is a distinct transcription factor with a basic-region leucine zipper structure, whose activity is regulated by alternative splicing in response to disruptions in endoplasmic reticulum (ER) homeostasis and the unfolded protein response (UPR) activation. XBP1 interacts with a key signaling component of the highly conserved UPR and is critical in determining cell fate when responding to ER stress in liver diseases. This review aims to elucidate the emerging roles and molecular mechanisms of XBP1 in liver pathogenesis, focusing on its involvement in DILI, viral liver infections, MASLD, fibrosis/cirrhosis, and liver cancer. Understanding the multifaceted functions of XBP1 in these liver diseases offers insights into potential therapeutic strategies to restore ER homeostasis and mitigate liver damage.

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  • 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
    Clinical and Molecular Hepatology.2026; 32(1): e29.     CrossRef
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    Yuhang Zhou, Bang Wang, Miaoxin Wu, Han Hong, Gaochao Li, Minhui Xu
    Scientific Reports.2025;[Epub]     CrossRef
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    Andrew Hakeem, Jop van Berlo, Xavier S. Revelo
    JACC: Basic to Translational Science.2025; 10(7): 101309.     CrossRef
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    Delan Huang, Fan Gu, Jingzhi Ma, Zhi Chen
    Biomedicines.2025; 13(11): 2663.     CrossRef
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    Rong He, Kecen Zhao
    Medicine.2025; 104(44): e45652.     CrossRef
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    Qian Xu, Tian Liang, Jiahe Li, Suzhen Wang, Hua Zhang, Julie Hollien, Takao Iwawaki, Chunlin Qin, Yongbo Lu
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Reply to Correspondence

Artificial intelligence, epidemiology, methodology, or others

Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clin Mol Hepatol 2024;30(4):1039-1041.
Published online September 24, 2024
DOI: https://doi.org/10.3350/cmh.2024.0801
  • 5,665 View
  • 38 Download

Letter to the Editor

Steatotic liver disease

Sex-specific associations of metabolic dysfunction-associated steatotic liver disease with cardiovascular outcomes
Meng-Yuan Miao, Jie-Qiong Lyu, Wei Jiang, Zhong-Yue Liu, Guo-Chong Chen
Clin Mol Hepatol 2025;31(1):e35-e38.
Published online September 20, 2024
DOI: https://doi.org/10.3350/cmh.2024.0719

Citations

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  • Sex‐Specific Impact of Metabolic Dysfunction‐Associated Fatty Liver Disease on Incident Cardiovascular Diseases and Mortality
    Mahsa Abbaszadeh, Farhad Hosseinpanah, Maryam Tohidi, Sahar Karimpour Reyhan, Maryam Mahdavi, Majid Valizadeh
    Endocrinology, Diabetes & Metabolism.2025;[Epub]     CrossRef
  • Implication of the Androgen Receptor in Muscle–Liver Crosstalk: An Overlooked Mechanistic Link in Lean-MASLD
    Eleni Myrto Trifylli, Christiana Charalambous, Nikolaos Spiliotopoulos, Nikolaos Papadopoulos, Anastasia Oikonomou, Spilios Manolakopoulos, Melanie Deutsch
    Livers.2025; 5(4): 65.     CrossRef
  • 5,984 View
  • 90 Download
  • 2 Web of Science
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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
  • 4,664 View
  • 93 Download

Editorial

Steatotic liver disease

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
Clin Mol Hepatol 2025;31(1):293-296.
Published online August 27, 2024
DOI: https://doi.org/10.3350/cmh.2024.0703

Citations

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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
  • The correlation between the polymorphism of lysolecithin acyltransferase (MBOAT7) rs641738 and liver fibrosis
    Yuxia Yang, Xiang Chen, Huiqin Zhang, Gang Yang, Xiaoyun Zhu, Xiujing Si, Feilong Chen, Yan Zhao, Feng Jin, Juanjuan Lu
    Personalized Medicine.2025; 22(2): 113.     CrossRef
  • Advancing precision medicine in metabolic dysfunction-associated steatotic liver disease
    Bryan A. Priego-Parra, Rocío Gallego-Durán, Berenice M. Román-Calleja, José Antonio Velarde-Ruiz Velasco, Manuel Romero-Gómez, Jordi Gracia-Sancho
    Trends in Endocrinology & Metabolism.2025; 36(11): 1000.     CrossRef
  • 5,930 View
  • 122 Download
  • Crossref

Original Article

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 Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC).
Result
s: 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 Tm6sf2167K 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.

Citations

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  • Association of Circadian Rhythms With the Risk of Chronic Liver Disease: Findings From a Large Prospective Study
    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
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    Jack Leslie, Kishore A. Krishnamurthy, Indresh K. Gopalsamy, Patricia Inacio, Meritxell Huch, Suchira Gallage, Fiona Oakley, Michele Vacca
    Nature Reviews Gastroenterology & Hepatology.2026;[Epub]     CrossRef
  • 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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    Mohammad Shafi Kuchay, Narendra Singh Choudhary, Bruno Ramos-Molina
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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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Editorial

Steatotic liver disease

Incretin-based therapy in the management of metabolic dysfunction-associated steatotic liver disease (MASLD): one piece of the puzzle: Editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: A network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clin Mol Hepatol 2024;30(4):649-652.
Published online July 23, 2024
DOI: https://doi.org/10.3350/cmh.2024.0558

Citations

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  • AMPK Activation and Lipid Homeostasis Regulation in MASLD: Investigating the Hepatoprotective and Anti‐Inflammatory Effects of Meta‐Capridin Medium‐Chain Triglycerides
    Alireza Doagoo, Sajad Ehtiati, Reza Ataei kachouei, Seyyed Hossein Khatami, Shima Rajaei, Maral Jalilzadeh, Nastaran Hamed, Fatemeh Namvarjah, Reyhane Ahmadzade, Marjan Ajami, Farzaneh Salmani, Somayeh Mahmoodi Baram, Mitra Rezaei, Majid Sirati-Sabet, Hoj
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  • Evaluating causal protective effect of dual GLP-1R/GIPR agonists on MASLD: A Mendelian randomization and colocalization study
    Yangke Cai, Siyuan Xie, Liyi Xu, Jiamin Chen, Jianting Cai
    European Journal of Pharmacology.2025; 1005: 178088.     CrossRef
  • Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
    Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
    Clinical and Molecular Hepatology.2024; 30(4): 1039.     CrossRef
  • Correspondence to editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
    Hayeon Kim, Min Jeong Park, Myeong Gyu Kim, Kyungim Kim
    Clinical and Molecular Hepatology.2024; 30(4): 989.     CrossRef
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Correspondence

Steatotic liver disease

The role of SPP1 in MASLD pathogenesis: Therapeutic insights into ursolic acid’s mechanisms of action: Correspondence to editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic liver disease”
Yiyuan Zheng, Zhekun Xiong, Lina Zhao, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Fengbin Liu, Yong Li
Clin Mol Hepatol 2024;30(4):1019-1022.
Published online July 8, 2024
DOI: https://doi.org/10.3350/cmh.2024.0471

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  • Single‑cell RNA sequencing analysis of intrahepatic cholangiocarcinoma reveals SPP1 facilitates disease progression via interaction with CD4+ T cells
    Xian Lin, Huanyan Peng, Ke Liu, Wenqi Chen, Ximing Shao, Chun Ning, Hongchang Li, Dongye Yang
    Oncology Letters.2025; 30(2): 1.     CrossRef
  • 5,508 View
  • 73 Download
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Editorial

Steatotic liver disease

Ursolic acid: A promising therapeutic agent for metabolic dysfunction-associated steatotic liver disease via inhibition of SPP1-induced Th17 cell differentiation: Editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic liver disease”
So Jung Kim, Jeongeun Hyun
Clin Mol Hepatol 2024;30(4):709-713.
Published online June 11, 2024
DOI: https://doi.org/10.3350/cmh.2024.0412

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  • Ursolic acid in colorectal cancer: mechanisms, current status, challenges, and future research directions
    Huici Zhang, Xiaoyu Zhang, Xijun Ma, Xuan Wang
    Pharmacological Reports.2025; 77(1): 72.     CrossRef
  • Therapeutic applications of ursolic acid: a comprehensive review and utilization of predictive tools
    Sherien M. Bakry, Riham A. El-Shiekh, Shymaa Hatem, Asmaa A. Mandour, Ahmed M. El-Dessouki, Abeer Bishr, Heba Elosaily, Ahmed F. Mohamed, Shaza M. Elhusseiny
    Future Journal of Pharmaceutical Sciences.2025;[Epub]     CrossRef
  • Negative Correlation Between Secreted Phosphoprotein 1 and the Treg/Th17 Ratio in Non-Valvular Atrial Fibrillation
    Chao-Jun Yang, Bo Fu, Yi-Fan Huang, Jing-Yi Wu, Zhi-Xing Fan, Ya-Hui Li
    Reviews in Cardiovascular Medicine.2025;[Epub]     CrossRef
  • The role of SPP1 in MASLD pathogenesis: Therapeutic insights into ursolic acid’s mechanisms of action: Correspondence to editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic
    Yiyuan Zheng, Zhekun Xiong, Lina Zhao, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Fengbin Liu, Yong Li
    Clinical and Molecular Hepatology.2024; 30(4): 1019.     CrossRef
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Original Article

Steatotic liver disease

Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic liver disease
Yiyuan Zheng, Lina Zhao, Zhekun Xiong, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Yugang Fu, Simin Gu, Chong Chen, Jiacheng Li, Yingying Zhu, Jing Liu, Fengbin Liu, Yong Li
Clin Mol Hepatol 2024;30(3):449-467.
Published online April 16, 2024
DOI: https://doi.org/10.3350/cmh.2024.0047
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) has become an increasingly important health challenge, with a substantial rise linked to changing lifestyles and global obesity. Ursolic acid, a natural pentacyclic triterpenoid, has been explored for its potential therapeutic effects. Given its multifunctional bioactive properties, this research further revealed the pharmacological mechanisms of ursolic acid on MASLD.
Methods
Drug target chips and bioinformatics analysis were combined in this study to explore the potential therapeutic effects of ursolic acid on MASLD. Molecular docking simulations, surface plasmon resonance analyses, pull-down experiments, and co-immunoprecipitation assays were used to verify the direct interactions. Gene knockdown mice were generated, and high-fat diets were used to validate drug efficacy. Furthermore, initial CD4+ T cells were isolated and stimulated to demonstrate our findings.
Result
s: In this study, the multifunctional extracellular matrix phosphorylated glycoprotein secreted phosphoprotein 1 (SPP1) was investigated, highlighting its capability to induce Th17 cell differentiation, amplifying inflammatory cascades, and subsequently promoting the evolution of MASLD. In addition, this study revealed that in addition to the canonical TGF-β/IL-6 cytokine pathway, SPP1 can directly interact with ITGB1 and CD44, orchestrating Th17 cell differentiation via their joint downstream ERK signaling pathway. Remarkably, ursolic acid intervention notably suppressed the protein activity of SPP1, suggesting a promising avenue for ameliorating the immunoinflammatory trajectory in MASLD progression.
Conclusions
Ursolic acid could improve immune inflammation in MASLD by modulating SPP1-mediated Th17 cell differentiation via the ERK signaling pathway, which is orchestrated jointly by ITGB1 and CD44, emerging as a linchpin in this molecular cascade.

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    Jianxiang Jin, Yuping Zhang, Yiping Huang
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    Hanlin Xu, Zhechen Liu, Xiaofeng Zhou, Xiaoxi Ji, Xingwang Liu, Xiaoxia Zhu, Liwei Lu, Nicola Dalbeth, Rui He, Yinghui Hua
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    Chao-Jun Yang, Bo Fu, Yi-Fan Huang, Jing-Yi Wu, Zhi-Xing Fan, Ya-Hui Li
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    Changpeng Hu, Ming Qin, Wenjing Lai, Huyue Zhou, Chengsha Yuan, Yafeng Liu, Yue Dai, Mengmeng Yang, Min Hu, Xuan Wang, Menglin Luo, Rong Zhang, Guobing Li
    Journal for ImmunoTherapy of Cancer.2025; 13(11): e012586.     CrossRef
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  • The role of SPP1 in MASLD pathogenesis: Therapeutic insights into ursolic acid’s mechanisms of action: Correspondence to editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against metabolic dysfunction-associated steatotic
    Yiyuan Zheng, Zhekun Xiong, Lina Zhao, Chaoyuan Huang, Qiuhong Yong, Dan Fang, Fengbin Liu, Yong Li
    Clinical and Molecular Hepatology.2024; 30(4): 1019.     CrossRef
  • Complex Inhibitory Activity of Pentacyclic Triterpenoids against Cutaneous Melanoma In Vitro and In Vivo: A Literature Review and Reconstruction of Their Melanoma-Related Protein Interactome
    Arseny D. Moralev, Marina A. Zenkova, Andrey V. Markov
    ACS Pharmacology & Translational Science.2024; 7(11): 3358.     CrossRef
  • Ursolic acid: A promising therapeutic agent for metabolic dysfunction-associated steatotic liver disease via inhibition of SPP1-induced Th17 cell differentiation: Editorial on “Ursolic acid targets secreted phosphoprotein 1 to regulate Th17 cells against
    So Jung Kim, Jeongeun Hyun
    Clinical and Molecular Hepatology.2024; 30(4): 709.     CrossRef
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    Han Zhang, Yixian Wang, Mingyu Liu, Yao Qi, Shikai Shen, Qingwei Gang, Han Jiang, Yu Lun, Jian Zhang
    Journal of Cellular and Molecular Medicine.2024;[Epub]     CrossRef
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Letter to the Editor

Steatotic liver disease

Changing from NAFLD to MASLD: Prevalence and progression of ASCVD risk are similar between NAFLD and MASLD in Asia
Hiroyuki Suzuki, Tsubasa Tsutsumi, Machiko Kawaguchi, Keisuke Amano, Takumi Kawaguchi
Clin Mol Hepatol 2024;30(3):577-579.
Published online March 6, 2024
DOI: https://doi.org/10.3350/cmh.2024.0157

Citations

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    Takashi Omatsu, Masahiro Koseki, Kaori Ito, Ayami Saga, Hiroshi Sawabe, Katsunao Tanaka, Hiroyasu Inui, Takeshi Okada, Makoto Nishida, Hirokazu Takahashi, Shinichi Aishima, Yoshihiro Kamada, Hiroshi Yoshida, Yasushi Sakata
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    Yea-Chan Lee, Hye Sun Lee, Soyoung Jeon, Yae-Ji Lee, Yu-Jin Kwon, Ji-Won Lee
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    Satoko Tajirika, Takao Miwa, Masahito Shimizu, Mayumi Yamamoto
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  • Metabolic dysfunction-associated steatotic liver disease and risk of four intrahepatic and extrahepatic diseases
    Yiyuan Xiao, Sihua Xu, Wenyan Hu, Jiapeng Huang, Deke Jiang, Rong Na, Zhaoqing Yin, Jingjing Zhang, Haitao Chen
    Annals of Hepatology.2025; 30(1): 101750.     CrossRef
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    Yue Wang, Sherlot Juan Song, Yichong Jiang, Jimmy Che-To Lai, Grace Lai-Hung Wong, Vincent Wai-Sun Wong, Terry Cheuk-Fung Yip
    Clinical and Molecular Hepatology.2025; 31(Suppl): S51.     CrossRef
  • Pathogenic Mechanisms of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)-Associated Hepatocellular Carcinoma
    Toru Nakamura, Atsutaka Masuda, Dan Nakano, Keisuke Amano, Tomoya Sano, Masahito Nakano, Takumi Kawaguchi
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    Xinyue Sun, Jinge Wu, Huiqian Lv, Ben Wang, Xuelian Chen, Wenjing Ren, Xiulian Miao, Yan Guo, Xiaocen Kong, Huihui Xu, Zeqing Bao, Yong Xu, Zilong Li
    Metabolism.2025; 168: 156242.     CrossRef
  • Pemafibrate Reduced Liver Stiffness in Patients with Metabolic Dysfunction-associated Steatotic Liver Disease Complicated with Hyperlipidemia and Liver Fibrosis with a Fibrosis-4 Index Above 1.3
    Tatsuki Ichikawa, Mio Yamashima, Shinobu Yamamichi, Makiko Koike, Yusuke Nakano, Hiroyuki Yajima, Osamu Miyazaki, Tomonari Ikeda, Takuma Okamura, Naohiro Komatsu, Sayuri Sugio, Miruki Yoshino, Hisamitsu Miyaaki
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  • All-cause and disease-specific mortality in young adults with MASLD: A nationwide cohort study
    Jeayeon Park, Goh Eun Chung, Su Jong Yu, Yoon Jun Kim, Jung-Hwan Yoon, Kyungdo Han, Eun Ju Cho
    JHEP Reports.2025; 7(9): 101477.     CrossRef
  • Evolving Public Attention to Steatotic Liver Disease: A 20‐Year Analysis (2004–2024)
    Pojsakorn Danpanichkul, Charat Thongprayoon, Kanokphong Suparan, Donghee Kim, Ornpailin Wanichthanaolan, Phuuwadith Wattanachayakul, Yanfang Pang, Mark D. Muthiah, Anand V. Kulkarni, Ju Dong Yang, Apichat Kaewdech, Wisit Cheungpasitporn, Karn Wijarnpreech
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  • Impact of Continuous Nutritional Counseling on Liver Function and Body Composition in Patients with MASLD/MASH
    Shiho Asai, Naoto Kawabe, Akemi Ito, Teiji Kuzuya, Eizaburo Ohno, Takuji Nakano, Kazunori Nakaoka, Hiroyuki Tanaka, Yuka Ochi, Sayuri Miyaji, Sayaka Morisaki, Yoshiki Hirooka
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Editorial

Steatotic liver disease

Clinical impact of five cardiometabolic risk factors in metabolic dysfunction-associated steatotic liver disease (MASLD): Insights into regional and ethnic differences
Joo Hyun Oh, Dae Won Jun
Clin Mol Hepatol 2024;30(2):168-170.
Published online March 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0140

Citations

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    Hideki Fujii, Michihiro Iwaki, Yoshihiro Kamada
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  • Reply to correspondence on “Prognosis of biopsy-confirmed metabolic dysfunction-associated steatotic liver disease: A sub-analysis of the CLIONE study”
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  • Crossref

Letter to the Editor

Steatotic liver disease

Similar respiratory function including chronic obstructive pulmonary disease between non-alcoholic fatty liver disease and metabolic dysfunction-associated steatotic liver disease
Tsubasa Tsutsumi, Dan Nakano, Machiko Kawaguchi, Hirokazu Takahashi, Takumi Kawaguchi
Clin Mol Hepatol 2024;30(2):266-268.
Published online January 30, 2024
DOI: https://doi.org/10.3350/cmh.2024.0028

Citations

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  • Role of noninvasive tests in the prognostication of metabolic dysfunction-associated steatotic liver disease
    Yue Wang, Sherlot Juan Song, Yichong Jiang, Jimmy Che-To Lai, Grace Lai-Hung Wong, Vincent Wai-Sun Wong, Terry Cheuk-Fung Yip
    Clinical and Molecular Hepatology.2025; 31(Suppl): S51.     CrossRef
  • Is type 2 diabetes a link between lung function and metabolic dysfunction–associated steatotic liver disease? Insights from population studies and Mendelian randomization
    Runmin Cao, Yurun Zhang, Ling Cao, Honghe Jiang
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  • In-silico identification and experimental validation of shared genes and pathways to decipher the molecular links between COPD and MASLD
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  • Crossref

Snapshot

Steatotic liver disease

Evaluating the therapeutic efficacy of NAD supplementation in management of metabolic dysfunction-associated steatotic liver disease: Key considerations
Xinyi Lu, Rui Yang, Yu Chen, Daozhen Chen
Clin Mol Hepatol 2024;30(3):582-584.
Published online December 29, 2023
DOI: https://doi.org/10.3350/cmh.2023.0555

Citations

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  • β-Nicotinamide Mononucleotide protects against endotoxemia-induced myocardial injury through Sirt5-dependent desuccinylation of succinate dehydrogenase
    Hongmei Tao, Qian Dong, Yang Long, Ling Liu, Shu Qin, Yu Wang
    European Journal of Pharmacology.2026; 1015: 178562.     CrossRef
  • Immunonutrition: Another Player on the MASLD Field
    Iván López-Méndez, Misael Uribe, Eva Juárez-Hernández
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Special Review

Steatotic liver disease

Critical appraisal of metabolic dysfunction-associated steatotic liver disease: Implication of Janus-faced modernity
Gi-Ae Kim, Joon Ho Moon, Won Kim
Clin Mol Hepatol 2023;29(4):831-843.
Published online August 25, 2023
DOI: https://doi.org/10.3350/cmh.2023.0277
The existing term non-alcoholic fatty liver disease (NAFLD) has raised substantial concerns due to its inherent disadvantages of using exclusionary diagnostic criteria and the stigmatizing word ‘fatty.’ Three pan-national liver associations set out to explore a new nomenclature to replace both NAFLD and its suggested alternative, metabolic (dysfunction)-associated fatty liver disease (MAFLD). They surveyed if a change in nomenclature and/or definition is favored and which nomenclature best communicates disease characteristics and increases awareness. In lieu of NAFLD/MAFLD, metabolic dysfunction-associated steatotic liver disease (MASLD) has been chosen, and an umbrella term, steatotic liver disease (SLD), encompassing the whole spectrum of liver disease, has been proposed. It has been suggested that cardiometabolic risk factors should be considered when categorizing SLD patients. Furthermore, a new subcategory, MASLD with increased alcohol intake (MetALD), casts light on a neglected group of patients with moderate or more alcohol consumption. The importance of metabolic dysfunction was acknowledged in this new nomenclature, but the precise contribution of metabolic dysfunction and alcohol consumption to the development and progression of SLD remains unclear. Herein, we review hepatologists’ and endocrinologists’ perspectives on the new nomenclature, along with its possible impact on clinical practice. Although it is premature to predict the settlement of the new nomenclature, this review may help build more evidence for a soft landing of it in the future.

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  • Impact of healthy lifestyles on the risk of metabolic dysfunction‐associated steatotic liver disease among adults with comorbid hypertension and diabetes: Novel insight from a largely middle‐aged and elderly cohort in South China
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    Clinical and Molecular Hepatology.2025; 31(2): 382.     CrossRef
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    Clinical and Molecular Hepatology.2025; 31(2): 628.     CrossRef
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    Frontiers in Pharmacology.2025;[Epub]     CrossRef
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    Suebin Park, Su-Hyeon Lee, Se-eun Han, Beom Kyung Kim, Byungjin Hwang
    Hepatology Communications.2025;[Epub]     CrossRef
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    Hepatology International.2025;[Epub]     CrossRef
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