Clinical and Molecular Hepatology

"Metabolic dysfunction-associated steatotic liver disease"

Original Article

The natural history and individualized prediction of liver stiffness-based fibrosis risk in metabolic dysfunction-associated steatotic liver disease: Yu Shi, Ruoqi Zhou, Seung Up Kim, Terry Cheuk-Fung Yip, Salvatore Petta, Elisabetta Bugianesi, Masato Yoneda, Manuel Romero-Gomez, Emmanuel Tsochatzis, Philip Newsome, Hannes Hagström, George Boon-Bee Goh, Wah-Kheong Chan, José-Luis Calleja, Jerome Boursier, Arun J. Sanyal, Jian-Gao Fan, Laurent Castera, Victor de Lédinghen, Michelle Lai, Xiao-Dong Zhou, Vincent Wai-Sun Wong, Ming-Hua Zheng, on behalf of VCTE-Prognosis Study Group; Clin Mol Hepatol 2026;32(3):1333-1348.
Published online May 20, 2026; DOI: https://doi.org/10.3350/cmh.2026.0279

Abstract
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Background/Aims
Liver stiffness measurement (LSM) is a key tool for risk stratification in metabolic dysfunction-associated steatotic liver disease (MASLD), yet static thresholds fail to capture dynamic transition across risk strata. We aimed to characterize LSM-risk transitions and develop a time-updated, individualized model for predicting state transitions, liver-related events and death (LREs/death).
Methods
In a real-world MASLD cohort, we applied a multi-state, time-homogeneous Markov model to quantify annual transition probabilities and mean state occupancy times across LSM-defined low-, intermediate-, and high-risk strata. A Markov model incorporating age, sex, type 2 diabetes (T2D), hypertension was used to generate individualized, time-updated risk trajectories and probabilities of LREs/death.
Results
Among 11,514 MASLD individuals with ≥2 vibration-controlled transient elastography assessments, the low-risk category demonstrated notable stability, with 92% remaining unchanged at 1 year and a mean occupancy time of 8.43 years (95% confidence interval [CI] 7.94–8.95). Contrarily, the intermediate-risk category was highly dynamic, with only 39% remaining unchanged after 1 year and a mean occupancy time of 0.92 years (95% CI 0.88–0.96). T2D, hypertension, and obesity substantially shorten low-risk occupancy time, whereas antidiabetic medication was associated with more favorable transitions. Finally, we developed a dynamic, multi-state Markov model integrating longitudinal LSM-defined risk states with relevant covariates to generate individualized predictions of state transitions and risks of LREs/death.
Conclusions
LSM-based strata in MASLD represent distinct and meaningful dynamic trajectories. In particular, the marked instability of the intermediate-risk state supports more frequent reassessment. By quantifying transition pathways and time-updated risks of LREs/death, this model may inform the personalized surveillance intervals and risk-adapted management.

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Reply to Correspondence

Reply to correspondence on “Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis”: Yang-Hyun Baek; Clin Mol Hepatol 2026;32(3):e439-e440.
Published online January 27, 2026; DOI: https://doi.org/10.3350/cmh.2026.0068

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Editorials

A new lens on ferroptosis in liver disease: Near-infrared fluorescent probe of lipid peroxidation-driven microenvironmental remodeling: Editorial on “Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes”: Yunseo Bong, Wonhyo Seo; Clin Mol Hepatol 2026;32(3):1425-1428.
Published online January 27, 2026; DOI: https://doi.org/10.3350/cmh.2026.0003

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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; Clin Mol Hepatol 2026;32(3):1429-1432.
Published online January 9, 2026; DOI: https://doi.org/10.3350/cmh.2025.1482

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Bacteroides eggerthii: a new human gut probiotic against metabolic dysfunction-associated steatotic liver disease: Editorial on “Bacteroides eggerthii ameliorates metabolic dysfunction-associated steatotic liver disease through host–microbe signaling and highlights 2-hydroxyisocaproate as a potential effector”: Harry Cheuk-Hay Lau, Jun Yu; Clin Mol Hepatol 2026;32(3):1400-1404.
Published online December 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.1349

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Original Articles

Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes: 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.
Results
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.

Citations

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Targeting ferroptosis to halt MASLD and MASH
Fudi Wang
Trends in Endocrinology & Metabolism.2026;[Epub] CrossRef

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Crossref

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.
Results
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.

Citations

Citations to this article as recorded by

Are FIB-4 and liver stiffness measurement interchangeable for HCC risk stratification in MASLD?
Yimeng Zhou, Xue Meng
JHEP Reports.2026; : 101852. CrossRef
High Prevalence of Metabolic Dysfunction–Associated Steatohepatitis With Significant Fibrosis in Primary Care and Endocrinology Clinics
Srilaxmi Kalavalapalli, Eddison Godinez Leiva, Andrea Ortiz Rocha, Anu Sharma, Diana Barb, Nathaly Cuervo‐Pardo, Kelly Y. Chun, Toni R. Prezant, Margery A. Connelly, Jens T. Rosenberg, Joseph R. Grajo, Fernando Bril, Kenneth Cusi
Diabetes, Obesity and Metabolism.2026; 28(7): 6184. CrossRef
The Evolution of MASLD Management: From Revised Nomenclature to Disease-Modifying Therapies
Karolina Kornatowska, Szymon Kopciał, Mateusz Wiekiera, Adrianna Wiekiera, Paweł Budzik, Mateusz Tyniec, Kamal Morshed
Gastroenterology Insights.2026; 17(2): 33. CrossRef

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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.
Results
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.

Citations

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The MASLD Journey in the General Population: Linkage‐to‐Care and Patient‐Reported Uptake of Fibrosis Risk Assessment
Joo Hyun Oh, Jun‐Hyuk Lee, Sang Bong Ahn, Eunjoo Kwon, Eileen L. Yoon, Hyo Young Lee, Seon Cho, Dae Won Jun
Liver International.2026;[Epub] CrossRef

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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.
Results
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.

Citations

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Letter to the Editor: Circadian and microbial misalignment in metabolic dysfunction-associated steatotic liver disease - mechanistic insights and chronotherapeutic potential
Christos Savvidis, Ioannis Ilias
World Journal of Experimental Medicine.2026;[Epub] CrossRef
Decoding the Gut–Fat–Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies
Zijin Sun, Wei Shao, Haojia Zhang, Kai Wang, Yongchao Liu, Rui Zhou
International Journal of Molecular Sciences.2026; 27(12): 5596. CrossRef

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Correspondences

Correspondence to editorial 2 on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”: Dongqin Yang, Yuli Lin, Chunhua Song, Ming Guan; Clin Mol Hepatol 2026;32(3):e342-e345.
Published online September 29, 2025; DOI: https://doi.org/10.3350/cmh.2025.1100

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Correspondence to editorial 1 on “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, Dongqin Yang, Zhihao Wu, Ming Guan, Chunhua Song; Clin Mol Hepatol 2026;32(3):e339-e341.
Published online September 29, 2025; DOI: https://doi.org/10.3350/cmh.2025.1086

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Editorials

ASB3 degrades the gateway to β-oxidation: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A”: Ho Jae Ryu, Ji Su Han, Ja Hyun Koo; Clin Mol Hepatol 2026;32(3):1379-1382.
Published online September 23, 2025; DOI: https://doi.org/10.3350/cmh.2025.1021

Citations

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TREM1-mediated macrophage activation drives voriconazole-induced hepatic steatosis: Diagnostic and therapeutic implications
Jing Liu, Mingxia Deng, Xiaoying He, Jing Ma, Li Zhang, Xi Yang, Jinyao Dai, Shaohua Dong, Yichun Zhang, Zhijuan Zhang, Shuaibing Ying, Haoyang Hu, Lushun Jiang, Yujing Wang, Yunqing Qiu, Yan Lou
Journal of Pharmaceutical Analysis.2026; 16(6): 101540. CrossRef

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Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyltransferase 1A”: Yueying Yang, Ying Yang, Yan Lu; Clin Mol Hepatol 2026;32(2):957-959.
Published online September 15, 2025; DOI: https://doi.org/10.3350/cmh.2025.1013

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Letters to the Editor

Letter to the editor on “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”: Chunyan Wang, Xu Han, Yinyan Li; Clin Mol Hepatol 2026;32(2):e167-e169.
Published online August 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0676

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Letter to the editor 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; Clin Mol Hepatol 2026;32(2):e139-e140.
Published online August 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.0875

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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.
Results
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.

Citations

Citations to this article as recorded by

Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver diseas
Yueying Yang, Ying Yang, Yan Lu
Clinical and Molecular Hepatology.2026; 32(2): 957. CrossRef
The first genome-wide association study on pediatric obesity in Taiwan
Hsin-Ru Wu, Ting-Yuan Liu, Chuan-Mu Chen, Fuu-Jen Tsai
Journal of the Formosan Medical Association.2026;[Epub] CrossRef

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538 Download
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Editorials

The other face of GWAS: Editorial on “Genome-wide interaction study with body mass index identifies CYP7A1 and GIPR as genetic modulators of metabolic dysfunction-associated steatotic liver disease”: Hyungtai Sim, Murim Choi; Clin Mol Hepatol 2026;32(2):928-930.
Published online July 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.0677

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Rethinking first-line screening in MASLD beyond the limitations of Fibrosis-4 index: Editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease”: Han Ah Lee, Young Youn Cho, Hyung Joon Kim; Clin Mol Hepatol 2026;32(2):921-923.
Published online June 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0678

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Letter to the Editor

Letter to the editor on “Genome-wide interaction study with BMI identifies CYP7A1 and GIPR as genetic modulators of MASLD”: Sheng Zheng; Clin Mol Hepatol 2026;32(2):e170-e171.
Published online June 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0656

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Editorials

GLP-1RA may open a new era for MASLD treatment: Editorial on “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”: Ye Feng, Chengfu Xu; Clin Mol Hepatol 2026;32(2):924-927.
Published online June 24, 2025; DOI: https://doi.org/10.3350/cmh.2025.0628

Citations

Citations to this article as recorded by

Correspondence to editorial on “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, Mindie H. Nguyen
Clinical and Molecular Hepatology.2026; 32(2): e219. CrossRef

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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

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

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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).
Results
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

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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; 20(2): 292. CrossRef
Impact of newer antihyperglycemic agents on hepatic complications: A systematic review and meta-analysis of data from 5.3 million patients with type 2 diabetes mellitus
Jiwon Yang, Yeongseok Hwang, Jin-Sung Ju, Seungbong Han, Jihyun An, Ju Hyun Shim
Hepatology.2026;[Epub] CrossRef
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Assaf Issachar, Talish Razi, Ilya Borochov, Hadar Duskin Bitan, Ronen Arbel
Diabetes, Obesity and Metabolism.2026; 28(7): 5704. CrossRef
Early cancer risk reduction after GLP-1RA use: Signal or bias?: Letter to the editor on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic l
Shio-Shin Jean, Chih-Cheng Lai
Clinical and Molecular Hepatology.2026; 32(2): e163. CrossRef
Letter to the editor on “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”
Chunyan Wang, Xu Han, Yinyan Li
Clinical and Molecular Hepatology.2026; 32(2): e167. CrossRef
Correspondence to letter to the editor 1 on “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, Mindie H. Nguyen
Clinical and Molecular Hepatology.2026; 32(2): e231. CrossRef
Correspondence to letter to the editor 2 on “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, Mindie H. Nguyen
Clinical and Molecular Hepatology.2026; 32(2): e249. CrossRef
Letter to the editor on “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”
Xingyu Yao
Clinical and Molecular Hepatology.2026; 32(2): e165. CrossRef
Correspondence to editorial on “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, Mindie H. Nguyen
Clinical and Molecular Hepatology.2026; 32(2): e219. CrossRef
Reply to correspondence on “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”
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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

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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

Abstract
PDF

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.

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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

9,432 View
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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

6,727 View
55 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

Citations

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Comparison of the identification and practicability of non-invasive diagnostic indicators under NAFLD, MAFLD and MASLD in China: a cross-sectional study
Xin-Yun Tan, Hui-Hui Zou, Xinjuan Huang, Man-Jie Guo, Ruo-Ling Yu, Xue-Lian Liu, Ting Peng, Xuan Yang, Chun-Xiang Qin
BMJ Open.2026; 16(4): e094809. CrossRef

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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

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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

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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

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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

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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

Abstract
PDF

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.
Results
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.

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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

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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.

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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

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Published online October 11, 2024; DOI: https://doi.org/10.3350/cmh.2024.0823

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Artificial intelligence, epidemiology, methodology, or others

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Abstract
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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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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

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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

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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

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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

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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”
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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 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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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

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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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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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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
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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.
Results
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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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

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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

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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

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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

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Hongmei Tao, Qian Dong, Yang Long, Ling Liu, Shu Qin, Yu Wang
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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

Abstract
PDF

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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Gi-Ae Kim, Heejoon Jang, Moon Young Kim, Jeong Hwan Park, Jung Gil Park, Eun-Young Cho, Jae Yoon Jeong, Seogsong Jeong, Seul Ki Han, Heesu Kwon, Youngae Jung, Geum-Sook Hwang, Yu Rim Lee, Soo Young Park, Sang Gyune Kim, Won Kim
Gastroenterology.2026; 170(7): 1571. CrossRef
Liver Stiffness Directs Intrahepatic Cholesterol Accumulation Through YAP/TAZ in Metabolic Dysfunction‐Associated Steatotic Liver Disease
Na Young Lee, Myeung Gi Choi, Ho Jae Ryu, Young Jin Min, Seon Min Kim, Yeonseok Chung, Bo Kyung Koo, Yun Pyo Kang, Won Kim, Ja Hyun Koo
Advanced Science.2026;[Epub] CrossRef
Risk stratification for patients with MASLD based on cardiometabolic risk factors
Yiheng Zhang, Yan Wang, Yaping Xu, Xu Liu, Yundong Qu, Tao Li
BMC Public Health.2026;[Epub] CrossRef
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Alexander Plakida, Olga Iushkovska, Lidia Elżbieta Sierpińska
World Journal of Hepatology.2026;[Epub] CrossRef
Fucoxanthin Ameliorates MASLD by Directly Targeting GRP78 to Restore ER Homeostasis and Activate AMPK Signaling
Lin Zhang, Ruifen Zhang, Yu Wu, Binbin Chen, Chao Wang, Cheng Wang, Zhengshun Wen, Jingui Zhang, Haibin Tong, Liang Hong
Food Science & Nutrition.2026;[Epub] CrossRef
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Alice Biasin, Silvia Palmisano, Michela Abrami, Deborah Bonazza, Fabrizio Zanconati, Domenico Tierno, Federica Tonon, Nhung Hai Truong, Thanh Dang Minh, Ralf Weiskirchen, Fulvia Felluga, Bruna Scaggiante, Mario Grassi, Gabriele Grassi
International Journal of Molecular Sciences.2026; 27(9): 4040. CrossRef
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Qiyang Chen, Ruifang Xu, Linxue Qian, Yujiang Liu, Xiangdong Hu
European Journal of Gastroenterology & Hepatology.2026;[Epub] CrossRef
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Shakta Mani Satyam, Mohamed El-Tanani, Akheruz Zaman Ahmed, Manfredi Rizzo, Dimitrios Patoulias, Prakashchandra Shetty Kanyana, Kalyan Chakravarthi Kosuri, Rashmi Kumari, Sainath Prabhakar
Current Pharmaceutical Design.2026; 32(20): 1592. CrossRef
Comparison of NAFLD, MAFLD, and MASLD Prevalence and Clinical Characteristics in Asia Adults
Xinjuan Huang, Ruoling Yu, Xinyun Tan, Manjie Guo, Yuanqin Xia, Huihui Zou, Xuelian Liu, Chunxiang Qin
Journal of Clinical and Experimental Hepatology.2025; 15(1): 102420. CrossRef
Letter: Towards Better Intervention Strategies for MASLD and MetALD—What Are We Missing? Authors' Reply
Yewan Park, Jooyi Jung, Gi‐Ae Kim
Alimentary Pharmacology & Therapeutics.2025; 61(2): 400. CrossRef
Statin use and liver-related prognosis among patients with MASLD
Byungyoon Yun, Heejoo Park, Jian Lee, Beom Kyung Kim, Jin-Ha Yoon
JHEP Reports.2025; 7(4): 101313. CrossRef
Diet quality and physical activity affect metabolic dysfunction-associated steatotic liver disease, metabolic dysfunction and etiology-associated steatohepatitis, and compensated advanced chronic liver disease among United States adults: NHANES 2017–2020
Peng Wang, Bingxin Xia, Shuang Wang
Frontiers in Nutrition.2025;[Epub] CrossRef
Optimal BMI cutoff for lean MASLD/MetALD and adverse hepatic outcomes in East-Asian populations
Byungyoon Yun, Juyeon Oh, Heejoo Park, Beom Kyung Kim, Jin-Ha Yoon
European Journal of Internal Medicine.2025; 133: 141. CrossRef
Cardiovascular Risk From Metabolic Dysfunction-Associated Steatotic Liver Disease, Cardiometabolic Risk Factor Count, and Their Longitudinal Changes: A Nationwide Cohort Study
Hyeok-Hee Lee, Han Ah Lee, Eun-Jin Kim, Hwi Young Kim, Hyeon Chang Kim, Sang Hoon Ahn, Hokyou Lee, Seung Up Kim
American Journal of Gastroenterology.2025; 120(10): 2321. 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
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
Clinical and Molecular Hepatology.2025; 31(1): e35. CrossRef
Cigarette Smoke Contributes to the Progression of MASLD: From the Molecular Mechanisms to Therapy
Jiatong Xu, Yifan Li, Zixuan Feng, Hongping Chen
Cells.2025; 14(3): 221. CrossRef
Prognostic and predictive effects of new steatotic liver disease nomenclatures: a large population‐based study
Huixian Zeng, Letian Fang, Zhiyu Yang, Xinyu Zhao, Hongsen Chen, Puyi Xing, Zheyun Niu, Zheng Li, Zishuai Li, Jiayi Zhao, Wenbin Liu, Chunxia Jing, Hong You, Guangwen Cao
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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
Dapansutrile Regulates Mitochondrial Oxidative Stress and Reduces Hepatic Lipid Accumulation in Diabetic Mice
Ying Wu, Jiaqiang Zhou
Current Issues in Molecular Biology.2025; 47(3): 148. CrossRef
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Yoko UEBA, Kaori IKEDA, Yasuharu TABARA, Takeo NAKAYAMA, Daisuke TANAKA, Yoshimitsu TAKAHASHI, Shinji KOSUGI, Kazuya SETOH, Takahisa KAWAGUCHI, Fumihiko MATSUDA, Nobuya INAGAKI
Journal of Nutritional Science and Vitaminology.2025; 71(1): 25. 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
European Journal of Gastroenterology & Hepatology.2025; 37(5): 652. CrossRef
Impact of binge drinking on alcoholic liver disease
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Archives of Pharmacal Research.2025;[Epub] CrossRef
Synbiotic combination of fructooligosaccharides and probiotics ameliorates the metabolic dysfunction-associated steatotic liver disease
Sang Yoon Lee, Su-Been Lee, Goo-Hyun Kwon, Seol Hee Song, Jeong Ha Park, Min Ju Kim, Jung A Eom, Kyeong Jin Lee, Sang Jun Yoon, Hyunjoon Park, Sung-Min Won, Jin-Ju Jeong, Ki-Kwang Oh, Young Lim Ham, Gwang Ho Baik, Dong Joon Kim, Satya Priya Sharma, Ki Tae
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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
Jun‐Yan Xi, Yi‐Jing Wang, Xiao‐Heng Li, Nuo‐Min Sun, Rui‐Qi Ming, Hua‐Ling Yan, Huan‐Le Cai, Jian‐Jun Bai, Yi‐Ning Xiang, Jing Gu, Xiao Lin, Gang Liu, Yuan‐Tao Hao
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Association Between Handgrip Strength and Cardiovascular Disease Risk in MASLD: A Prospective Study From UK Biobank
Tae Seop Lim, Sujin Kwon, Sung A. Bae, Hye Yeon Chon, Seol A. Jang, Ja Kyung Kim, Chul Sik Kim, Seok Won Park, Kyoung Min Kim
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Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
Alimentary Pharmacology & Therapeutics.2025; 61(11): 1785. CrossRef
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Jialin Ren, Min Wu
International Journal of Molecular Sciences.2025; 26(7): 3166. CrossRef
Linghe granules reduces hepatic lipid accumulation in Non-alcoholic fatty liver disease through regulating lipid metabolism and redox balance
Yuting Hu, Ni'ao Li, Rumian Zhang, Jia Wang, Dongdong Fang, Qianmei Zhou, Hua Zhang, Hong Cai, Yiyu Lu
Phytomedicine.2025; 141: 156654. CrossRef
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
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Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
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Reply to correspondence 1 on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
Yoon-su Ha, Won Kim, Seung-Jin Kim
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Yoon-su Ha, Won Kim, Seung-Jin Kim
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Raúl Gómez-Mendoza, Fabiola Sánchez-Hernández, Francisco Javier Valentin-Cortez, Norberto Chávez-Tapia
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Ruichen Yang, Qingqing Jiang, Wentao Liu, Furong Wang, Shiyi Cao
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New steatotic liver disease criteria diagnostic performance in an agricultural population in Chile
Maria Spencer-Sandino, Franco Godoy, Laura Huidobro, Danilo Alvares, Francisco Cruz, Claudia Marco, Macarena Garrido, Daniel Cabrera, Juan Pablo Arab, Marco Arrese, Francisco Barrera, Catterina Ferreccio
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Chronic Kidney Disease Risk Associated With Metabolic Dysfunction‐Associated Steatotic Liver Disease: A Nationwide Cohort Study in Korea
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Association Between Meat Intake and Metabolic Dysfunction‐Associated Steatotic Liver Disease Incidence in a Korean Population From the Health Examinees Study
Uyangamaa Nyamsuren, Yuan Peng, Sangah Shin
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Rui-Qi Ye, Yi-Fan Chen, Chang Ma, Xi Cheng, Wei Guo, Sha Li
Biomedicine & Pharmacotherapy.2025; 188: 118191. CrossRef
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Clinical Gastroenterology and Hepatology.2025; 23(13): 2540. CrossRef
Chronic Inflammation and Immune Dysregulation in Metabolic-Dysfunction-Associated Steatotic Liver Disease Progression: From Steatosis to Hepatocellular Carcinoma
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Biomedicines.2025; 13(5): 1260. CrossRef
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Iván López-Méndez, Eva Juárez-Hernández, Juan Pablo Soriano-Márquez, Misael Uribe, Graciela Castro-Narro
Expert Review of Gastroenterology & Hepatology.2025; 19(7): 755. CrossRef
Future Perspectives of Liver Research in the Asia‐Pacific Region: Focus on Hepatitis B and C
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Journal of Gastroenterology and Hepatology.2025; 40(8): 1855. CrossRef
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Yutian Zhang, Tianlin Wang, Junquan Han, Jielin Song, Chaoshuai Yang, Lei Liang, Huizhen Li, Hong Wang
Frontiers in Pharmacology.2025;[Epub] CrossRef
Laminin γ2 accelerates non-alcoholic fatty liver disease progression by enhancing lipid accumulation and fibrogenesis in hepatocytes
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Biochemical and Biophysical Research Communications.2025; 777: 152266. CrossRef
Dietary ω-3 polyunsaturated fatty acid intake improves skeletal muscle mass in patients with metabolic dysfunction-associated fatty liver disease: A nationwide cross-sectional study
Li-Zhan Bie, Chao Wu, Jia-Lu Wang
World Journal of Hepatology.2025;[Epub] CrossRef
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Donghee Kim, Rohit Loomba, Aijaz Ahmed
Clinical and Molecular Hepatology.2025; 31(3): e235. CrossRef
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Gut and Liver.2025; 19(4): 479. CrossRef
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Cristina Carresi, Antonio Cardamone, Vincenzo Musolino, Rocco Mollace, Annamaria Tavernese, Anna Rita Coppoletta, Micaela Gliozzi, Vincenzo Mollace
Biomedicine & Pharmacotherapy.2025; 190: 118375. CrossRef
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Gut and Liver.2025; 19(5): 639. CrossRef
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Phytomedicine.2025; 148: 157404. CrossRef
Paired snRNA-seq and scRNA-seq analysis of MASLD patients to identify early-stage markers for disease progression
Suebin Park, Su-Hyeon Lee, Se-eun Han, Beom Kyung Kim, Byungjin Hwang
Hepatology Communications.2025;[Epub] CrossRef
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Metabolism and Target Organ Damage.2025;[Epub] CrossRef
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Journal of Obesity & Metabolic Syndrome.2025; 34(4): 456. CrossRef
Steatotic Liver Disease Subtypes and Their Association with Colorectal Cancer Risk in Korea: A Nationwide Population-Based Study
Sang Yi Moon, Minkook Son, Jong Yoon Lee, Yeo Wool Kang, Myeongseok Koh
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Steatotic liver disease predicts cardiovascular disease and advanced liver fibrosis: A community-dwelling cohort study with 20-year follow-up
Hun Jee Choe, Joon Ho Moon, Won Kim, Bo Kyung Koo, Nam H. Cho
Metabolism.2024; 153: 155800. CrossRef
Clinical profiles and mortality rates are similar for metabolic dysfunction-associated steatotic liver disease and non-alcoholic fatty liver disease
Zobair M. Younossi, James M. Paik, Maria Stepanova, Janus Ong, Saleh Alqahtani, Linda Henry
Journal of Hepatology.2024; 80(5): 694. CrossRef
From Nonalcoholic Fatty Liver Disease to Metabolic Dysfunction-Associated Steatotic Liver Disease: Out with the Old, in with the New
Iyiad Alabdul Razzak, Mazen Noureddin, Hirsh Trivedi
Journal of Clinical Medicine.2024; 13(3): 880. CrossRef
Gut microbiota-derived indole compounds attenuate metabolic dysfunction-associated steatotic liver disease by improving fat metabolism and inflammation
Byeong Hyun Min, Shivani Devi, Goo Hyun Kwon, Haripriya Gupta, Jin-Ju Jeong, Satya Priya Sharma, Sung-Min Won, Ki-Kwang Oh, Sang Jun Yoon, Hee Jin Park, Jung A Eom, Min Kyo Jeong, Ji Ye Hyun, Nattan Stalin, Tae-Sik Park, Jieun Choi, Do Yup Lee, Sang Hak H
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Metabolic dysfunction‐associated steatotic liver disease and MetALD increases the risk of liver cancer and gastrointestinal cancer: A nationwide cohort study
Yewan Park, Jooyi Jung, Seungbong Han, Gi‐Ae Kim
Alimentary Pharmacology & Therapeutics.2024; 60(11-12): 1599. CrossRef
Metabolic dysfunction-associated steatotic liver disease: An opportunity for collaboration between cardiology and hepatology
Paolo Raggi, Jovana Milic, Marcella Manicardi, Felice Cinque, Mark G. Swain, Giada Sebastiani, Giovanni Guaraldi
Atherosclerosis.2024; 392: 117523. CrossRef
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Sumin Oh, Yang-Hyun Baek, Sungju Jung, Sumin Yoon, Byeonggeun Kang, Su-hyang Han, Gaeul Park, Je Yeong Ko, Sang-Young Han, Jin-Sook Jeong, Jin-Han Cho, Young-Hoon Roh, Sung-Wook Lee, Gi-Bok Choi, Yong Sun Lee, Won Kim, Rho Hyun Seong, Jong Hoon Park, Yeon
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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
Clinical and Molecular Hepatology.2024; 30(2): 266. CrossRef
Immunopathogenesis of liver fibrosis in steatotic liver disease
Chaerin Woo, Won-Il Jeong
Clinical and Molecular Hepatology.2024; 30(2): 299. CrossRef
Changing from NAFLD to MASLD: Similar prognosis of patients with HCC under atezolizumab/bevacizumab treatment between NAFLD and MASLD
Hiroyuki Suzuki, Shigeo Shimose, Hideki Iwamoto, Takashi Niizeki, Takumi Kawaguchi
Clinical and Molecular Hepatology.2024; 30(2): 263. CrossRef
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INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine).2024; 20(2): 120. CrossRef
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Chavdar S. Pavlov, Daria A. Teplyuk, Leonid B. Lazebnik, Aleksandr S. Ametov, Evgeniia Yu. Pashkova, Sergey M. Sorokoletov, Yury P. Uspenskiy, Svetlana V. Turkina, Elizaveta V. Ponomarenko, Aleksandr S. Maslakov
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Michail Kokkorakis, Emir Muzurović, Špela Volčanšek, Marlene Chakhtoura, Michael A. Hill, Dimitri P. Mikhailidis, Christos S. Mantzoros
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Sergio Gil-Rojas, Miguel Suárez, Pablo Martínez-Blanco, Ana M. Torres, Natalia Martínez-García, Pilar Blasco, Miguel Torralba, Jorge Mateo
Metabolites.2024; 14(6): 305. CrossRef
Are transmembrane 6 superfamily member 2 gene polymorphisms associated with steatohepatitis after pancreaticoduodenectomy?
Tomotaka Mori, Eisuke Ozawa, Ryu Sasaki, Akane Shimakura, Kosuke Takahashi, Yoko Kido, Yasuko Kanda, Satoshi Matsuo, Kazuaki Tajima, Asami Beppu, Yasuhiko Nakao, Masanori Fukushima, Masafumi Haraguchi, Satoshi Miuma, Hisamitsu Miyaaki, Tomohiko Adachi, Su
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Clinical and Molecular Hepatology.2024; 30(3): 577. CrossRef
Impacts of cardiometabolic risk factors and alcohol consumption on all-cause mortality among MASLD and its subgroups
Mengqi Li, Wenya Chen, You Deng, Wen Xie
Nutrition, Metabolism and Cardiovascular Diseases.2024; 34(9): 2085. CrossRef
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Nouhoum Bouare, Jean Delwaide
World Journal of Hepatology.2024; 16(7): 980. CrossRef
A New Korean Nomenclature for Steatotic Liver Disease

The Korean Journal of Gastroenterology.2024; 84(1): 1. CrossRef
Impact of Physical Activity on Overall Survival and Liver Cirrhosis Incidence in Steatotic Liver Disease: Insights from a Large Cohort Study Using Inverse Probability of Treatment Weighting
Keungmo Yang, Beom Sun Chung, Tom Ryu
Nutrients.2024; 16(15): 2532. CrossRef
Machine learning model reveals roles of interferon‑stimulated genes in sorafenib‑resistant liver cancer
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Role of Neutrophils in the Development of Steatotic Liver Disease
You-Jin Choi, Yeonsoo Kim, Seonghwan Hwang
Seminars in Liver Disease.2024; 44(03): 300. CrossRef
A New Korean Nomenclature for Steatotic Liver Disease

The Korean Journal of Medicine.2024; 99(4): 189. CrossRef
Emerging mechanisms of non-alcoholic steatohepatitis and novel drug therapies
Hao CHEN, Yang ZHOU, Haiping HAO, Jing XIONG
Chinese Journal of Natural Medicines.2024; 22(8): 724. CrossRef
Metabolic Dysfunction-Associated Steatotic Liver Disease Is Associated with Increased Risk of Kidney Cancer: A Nationwide Study
Juyeon Oh, Beom Kyung Kim, Jin-Ha Yoon, Hyung Ho Lee, Heejoo Park, Jian Lee, Youngsun Park, Byungyoon Yun, Jinsoo Chung
Cancers.2024; 16(18): 3161. CrossRef
A New Korean Nomenclature for Steatotic Liver Disease

Gut and Liver.2024; 18(5): 924. CrossRef
Serum isthmin-1 is a potential biomarker for metabolic dysfunction associated fatty liver disease in patients with metabolic syndrome and type 2 diabetes mellitus
Xiaohui Lei, HaiYan Chen, YuXin Xu, Zhuoran Yang, Lili Zhang, Cong Wang, Hu Du
BMJ Open Diabetes Research & Care.2024; 12(5): e004514. CrossRef
A new Korean nomenclature for steatotic liver disease

Clinical and Molecular Hepatology.2024; 30(Suppl): S214. CrossRef
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