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"SLD"

Reply to Correspondence

Reply to correspondence: Sodium-Glucose Cotransporter-2 Inhibitors and Liver Outcomes in Metabolic Dysfunction-associated Steatotic Liver Disease
Yang-Hsiang Lin, Ching-Chih Hu, Chih-Lang Lin
Received January 25, 2026  Accepted February 2, 2026  Published online February 5, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0123    [Accepted]
  • 63 View
  • 2 Download

Correspondence

Incorporating chronic kidney disease into the cost-effectiveness of MASLD treatment
Eileen L. Yoon, Jeong-Yeon Cho, Mimi Kim, Huiyul Park, Hye-Lin Kim, Dae Won Jun
Received January 20, 2026  Accepted January 24, 2026  Published online February 2, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0099    [Accepted]
  • 102 View
  • 5 Download

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]
  • 148 View
  • 9 Download

Correspondence

Key challenges in cost-effectiveness analyses of emerging MASLD therapies: adherence, adverse events, cardiometabolic benefits, and age-related uncertainty
Eileen L. Yoon, Jeong-Yeon Cho, Mimi Kim, Huiyul Park, Hye-Lin Kim, Dae Won Jun
Received January 13, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0059    [Accepted]
  • 117 View
  • 7 Download

Editorials

Rethinking Lean Metabolic Dysfunction-Associated Steatotic Liver Disease: Unrecognized Risk in Lean Populations
Donghee Kim, Anoushka Shenoy, Aijaz Ahmed
Received January 13, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0056    [Accepted]
  • 143 View
  • 17 Download
Reconciling Definitions, Phenotypes and Outcomes in Lean MASLD: Editorial on “Normal-weight MASLD: reclassification, characteristics, and adverse liver outcomes across diverse populations”
Shanshan Wu
Received January 2, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0004    [Accepted]
  • 126 View
  • 10 Download
Challenges and Innovations in MASLD and T2DM: Strengthening Personalized Medicine with SGLT2 Inhibitors
Yang-Hsiang Lin, Ching-Chih Hu, Chih-Lang Lin
Received January 2, 2026  Accepted January 17, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2026.0002    [Accepted]
  • 155 View
  • 9 Download

Original Article

DNMT1 Facilitates the Progression of MASLD by Impeding Transcription Mediated by HNF4α and PPARα
Hyun Ahm Sohn, Hanyong Go, Tae Hyeon An, Jun Min Lee, Hee-Jin Kim, Keeok Haam, Amal Magdy, Hyo-Jung Jung, Yang-Ji Shin, Hyun Jung Lim, Yujin Jeong, Yejin Bae, Youngae Jung, Seong-Hwan Park, Kyung Chan Park, Myeong Jun Song, Eun-Wie Cho, Eun-Soo Kwon, Jeong Hwan Park, Murim Choi, Geum-Sook Hwang, Dong Hyeon Lee, Stefano Romeo, Kyoung-Jin Oh, Won Kim, Mirang Kim
Received September 25, 2025  Accepted January 23, 2026  Published online January 27, 2026  
DOI: https://doi.org/10.3350/cmh.2025.1099    [Accepted]
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide. Aberrant DNA methylation, which is primarily maintained by DNA methyltransferase 1 (DNMT1), has been linked to metabolic dysregulation; however, its contribution to MASLD pathogenesis remains poorly defined. This study aimed to elucidate the role of DNMT1-mediated methylation in transcriptional regulation during MASLD progression and to determine whether DNMT1 inhibition can reverse disease-associated epigenetic and transcriptional alterations.
Methods
We conducted integrated analyses of the liver transcriptome (n = 131) and DNA methylome (n = 106) of patients with biopsy-proven MASLD. We evaluated the effect of DNMT1 inhibition with 5-aza-4′-thio-2′-deoxycytidine (Aza-TdC) on a diet-induced MASLD mouse model. Multiomics approaches, including DNA methylome profiling, lipidomics, bulk and single-nucleus RNA sequencing, and chromatin immunoprecipitation sequencing, were applied to elucidate the role of DNMT1-mediated DNA methylation in regulating pathogenic gene expression.
Results
DNA methylome profiling revealed increased methylation variability associated with increased DNMT1 expression in MASLD patients. DNMT1 inhibition ameliorated dysregulated lipid metabolism by reducing hepatic triacylglycerol accumulation and inflammation. Aza-TdC treatment partially reversed MASLD-related hypermethylation of hepatocyte nuclear factor 4 alpha (HNF4α)- and peroxisome proliferator-activated receptor alpha (PPARα)-regulated genes, restoring their transcriptional activity. Notably, Aza-TdC reactivated the gluconeogenic enzyme-encoding gene phosphoenolpyruvate carboxykinase 1 (PCK1), which was hypermethylated and transcriptionally repressed in MASLD. Targeted DNA methylation of the PCK1 promoter using CRISPRoff confirmed the direct epigenetic regulation of PCK1 expression.
Conclusions
Targeting DNMT1 may mitigate lipid dysregulation and inflammation by reversing hypermethylation and restoring HNF4α- and PPARα-dependent gene transcription, highlighting DNMT1 as a potential therapeutic target for MASLD.
  • 354 View
  • 61 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]
  • 391 View
  • 33 Download

Original Articles

MicroRNA isomiRs reveal novel pathways linked to disease activity and fibrosis in MASLD
Christian Brion, Stephen A. Hoang, Guangliang Wang, Faridodin Mirshahi, Jessie Ang, Matthew R. Long, Zheng Zhu, Bhanu Sakhamuri, Molly A. Srour, Mohammad S. Siddiqui, Amon Asgharpour, David J. Hayes, Neal C. Foster, David W. Salzman, Arun J. Sanyal
Received August 21, 2025  Accepted December 19, 2025  Published online December 26, 2025  
DOI: https://doi.org/10.3350/cmh.2025.0933    [Accepted]
Background/Aims
MicroRNA isoforms (isomiRs) broaden the regulatory landscape of canonical microRNAs, but their role in metabolic dysfunction-associated steatotic liver disease (MASLD) remains unknown. We aimed to characterize the hepatic isomiR landscape in MASLD and define their association with disease activity and fibrosis.
Methods
Small RNA (sRNA) sequencing was performed on liver biopsies from 79 patients across the histological spectrum of MASLD. IsomiRs were annotated and quantified. Their association to disease activity and fibrosis score was assessed by differential expression, ordinal regression, and machine learning. Parallel mRNA sequencing and pathway enrichment were used to map isomiR–mRNA interactions and regulatory networks, which was validated against an independent dataset.
Results
MiRNAs accounted for 75% of sRNAs in liver tissue, of which 67% were isomiRs. Across MASLD severity, 173 isomiRs correlated with disease activity and 58 with fibrosis stage. Key findings included a miR-122 isomiR uniquely targeting INSIG1 (cholesterol metabolism) and a miR-21 isomiR targeting PPARA and HMGCS2 (lipid and fibrosis pathways). Integration with mRNA data revealed 33 dysregulated pathways, including PPAR signaling, insulin resistance, and TGF-β response. Several novel isomiRs from miR-26b, let-7c, and miR-32 families were also linked to lipid metabolism and fibrosis progression.
Conclusions
IsomiRs represent the majority of hepatic miRNAs and uncover novel regulatory networks masked by canonical miRNA analysis. These findings provide new insights into the molecular heterogeneity of MASLD, highlight candidate pathways driving disease progression, and identify potential biomarker and therapeutic targets for precision hepatology.
  • 611 View
  • 57 Download
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.
Results
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
  • 1,095 View
  • 142 Download
  • Crossref
Comparative risk of fibrosis progression with sodium-glucose cotransporter-2 vs. dipeptidyl peptidase-4 inhibitors in metabolic dysfunction-associated steatotic liver disease and type 2 diabetes mellitus with low-to-intermediate fibrosis
Jonggi Choi, Daniel Fulop, Vy H. Nguyen, Eric Przybyszewski, Jiunn Song, Allison Carroll, Megan Michta, Erik Almazan, Tracey G. Simon, Raymond T. Chung
Clin Mol Hepatol 2026;32(1):305-317.
Published online November 11, 2025
DOI: https://doi.org/10.3350/cmh.2025.0825
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing cause of cirrhosis and its complications. Given its close association with type 2 diabetes mellitus (T2DM), evaluating whether sodium-glucose cotransporter-2 inhibitors (SGLT2is) can mitigate the progression of liver fibrosis is clinically important. We examined the association between SGLT2i use and liver fibrosis progression in patients diagnosed with MASLD and T2DM.
Methods
We conducted a target trial emulation study using a retrospective, active comparator new-user design among adults with MASLD, T2DM, and low-to-intermediate Fibrosis-4 (FIB-4≤2.67) scores who initiated treatment with either SGLT2is or dipeptidyl peptidase-4 inhibitors (DPP-4is) at Mass General Brigham or Asan Medical Center from 2013 to 2023. The primary outcome was the progression to advanced fibrosis (FIB-4>2.67), confirmed on ≥2 occasions within 1 year. The secondary outcome was the development of major adverse liver outcomes (MALO), including incident cirrhosis, decompensation events, hepatocellular carcinoma, or liver transplantation.
Results
Among 16,901 eligible patients, 2,571 propensity score-matched pairs were identified with balanced baseline characteristics. During follow-up (median, 3.7 years), fibrosis progression occurred at a rate of 3.46/100 personyears in SGLT2i users and 4.44 in DPP4i users. SGLT2i use was associated with a lower risk of fibrosis progression (HR 0.78, 95% CI 0.67–0.89; P<0.001). No significant difference in MALO incidence was observed. Subgroup analyses showed a consistent association among users of metformin, statins, and aspirin.
Conclusions
SGLT2i use was associated with reduced risk of fibrotic progression compared to DPP4i use in adults with MASLD and T2DM.
  • 1,724 View
  • 201 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.
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.
  • 1,012 View
  • 108 Download

Research Letter

Contemporary trends in extrahepatic mortality of chronic liver disease in the United States from 2014 to 2023
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed
Clin Mol Hepatol 2026;32(1):e24-e28.
Published online July 28, 2025
DOI: https://doi.org/10.3350/cmh.2025.0802
  • 2,776 View
  • 62 Download

Original Article

Genome-wide interaction study with body mass index identifies CYP7A1 and GIPR as genetic modulators of metabolic dysfunction-associated steatotic liver disease
Oveis Jamialahmadi, Endrina Mujica, Lowri Morris, Rosellina Margherita Mancina, Ester Ciociola, Sami F. Qadri, Samantha Maurotti, Francesco Malvestiti, Ruifang Li-Gao, Luisa Ronzoni, Federica Tavaglione, Hannah Maude, Amin Allalou, Anastasia Emmanouilidou, Umberto Vespasiani-Gentilucci, Frits Richard Rosendaal, Hannele Yki-Järvinen, Inês Cebola, Luca Valenti, Marcel den Hoed, Stefano Romeo
Clin Mol Hepatol 2025;31(4):1252-1268.
Published online June 2, 2025
DOI: https://doi.org/10.3350/cmh.2025.0159
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) may progress to liver inflammation, fibrosis, cirrhosis and hepatocellular carcinoma. So far, genome-wide association studies explain a small fraction of MASLD heritability.
Methods
We sought to identify novel genetic determinants of MASLD by exploring interactions between genetic variants and body mass index (BMI). First, we examined genome-wide interactions with BMI for circulating alanine aminotransferase (ALT) levels using UK Biobank data. For identified loci, we next examined associations with hepatic proton density fat fraction (PDFF) in 35,146 independent UK Biobank participants. Associations with PDFF were replicated in four independent European cohorts, followed by a phenome-wide association study. Finally, we used human liver epigenomic maps and CRISPR/Cas9 experiments in vitro and in vivo to functionally characterize the CYP7A1 locus.
Results
Thirteen loci interact with BMI for ALT (P<5E-8), including eight well-known genetic modulators of MASLD. Two loci—UBXN2B/CYP7A1 and GIPR—are additionally associated with PDFF. For the intronic rs34783010 in GIPR, the minor T allele is associated with lower BMI and higher HbA1c and liver triglyceride content in humans. The UBXN2B/CYP7A1 locus is associated with PDFF in four additional European cohorts. Epigenomic data and in vitro experiments in human liver cells prioritise rs10504255 and CYP7A1 as the functional effectors in this locus. Perturbation of CYP7A1 orthologues using CRISPR/Cas9 results in less liver fat in 10-day-old, metabolically challenged zebrafish larvae.
Conclusions
A genome-wide single nucleotide polymorphism×BMI design fuelled identification of two MASLD genes: CYP7A1 and GIPR.

Citations

Citations to this article as recorded by  Crossref logo
  • Human genetics of steatotic liver disease: insights into insulin resistance and lipid metabolism
    Rosellina M. Mancina, Luca Valenti, Stefano Romeo
    Nature Metabolism.2025; 7(11): 2199.     CrossRef
  • 4,827 View
  • 257 Download
  • 1 Web of Science
  • Crossref

Research Letter

Contemporary burden of mortality from chronic liver disease by sex and race/ethnicity in the United States
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
Clin Mol Hepatol 2025;31(3):e268-e272.
Published online May 8, 2025
DOI: https://doi.org/10.3350/cmh.2025.0384

Citations

Citations to this article as recorded by  Crossref logo
  • Advancing policy and practice in alcohol-associated liver disease and alcohol-attributable cancer: Correspondence to the editorial on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the Unite
    Pojsakorn Danpanichkul, Donghee Kim, Karn Wijarnpreecha, Amit G. Singal, Ju Dong Yang
    Clinical and Molecular Hepatology.2026; 32(1): e96.     CrossRef
  • Contemporary trends in extrahepatic mortality of chronic liver disease in the United States from 2014 to 2023
    Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed
    Clinical and Molecular Hepatology.2026; 32(1): e24.     CrossRef
  • Rising drug overdose deaths in chronic liver disease in the United States, 2015–2023
    Donghee Kim, Brittany B Dennis, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
    Clinical and Molecular Hepatology.2025; 31(3): e277.     CrossRef
  • Extrahepatic manifestation of metabolic dysfunction-associated steatotic liver disease
    Anoushka Shenoy, Aijaz Ahmed, Donghee Kim
    Metabolism and Target Organ Damage.2025;[Epub]     CrossRef
  • 8,348 View
  • 51 Download
  • 4 Web of Science
  • Crossref

Letter to the Editor

Letter to the editor on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”
Sisi Yang, Zhenxuan Ma
Clin Mol Hepatol 2026;32(1):e4-e6.
Published online March 7, 2025
DOI: https://doi.org/10.3350/cmh.2025.0153
  • 4,791 View
  • 40 Download

Correspondences

HCC predictors in routine practice for patients with chronic liver diseases: Correspondence to editorial on “High SAFE scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction associated steatotic liver disease”
Tung-Hung Su, Jia-Horng Kao
Clin Mol Hepatol 2026;32(1):e52-e54.
Published online February 26, 2025
DOI: https://doi.org/10.3350/cmh.2025.0187
  • 3,971 View
  • 28 Download

Steatotic liver disease

The burden of steatotic liver disease before and during the COVID-19 pandemic: Correspondence to editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
Clin Mol Hepatol 2025;31(2):e183-e185.
Published online February 17, 2025
DOI: https://doi.org/10.3350/cmh.2025.0152

Citations

Citations to this article as recorded by  Crossref logo
  • Reply to correspondence on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
    Jeayeon Park, Su Jong Yu
    Clinical and Molecular Hepatology.2025; 31(2): e221.     CrossRef
  • Neonatal liver-derived FTH1-enriched extracellular vesicles attenuate ferroptosis and ameliorate MASLD pathogenesis
    Xin Zeng, Wei Jiang, Tian Wu, Lan Li, Fudong Fu, Han Yao, Dongbo Wu
    Free Radical Biology and Medicine.2025; 240: 693.     CrossRef
  • Liver-Related COVID-19 Consequences: Dynamics of Liver Health in 2.5 Years
    Ieva Vanaga, Oksana Kolesova, Aleksandrs Kolesovs, Maija Radzina, Davis Simanis Putrins, Jelena Egle, Sniedze Laivacuma, Jelena Storozenko, Ludmila Viksna
    Journal of Clinical Medicine.2025; 14(21): 7604.     CrossRef
  • Prevalence of MASLD and fibrosis assessed by transient elastography in U.S. adolescents: insights from NHANES 2017-2023
    Jialin Wu, Junlong Huang, Shiyu Cao, Yang Lyu, Peiyao Yu, Tiejun Feng, Bonan Chen, Fuda Xie, Ge Zhang, Kangmin Zhuang, Aimin Li, Ka Fai To, Wei Kang
    Diabetology & Metabolic Syndrome.2025;[Epub]     CrossRef
  • 5,286 View
  • 17 Download
  • 3 Web of Science
  • Crossref

Steatotic liver disease

Addressing the burden of steatotic liver disease: The role of transient elastography: Correspondence to editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017-2023”
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
Clin Mol Hepatol 2025;31(2):e180-e182.
Published online February 13, 2025
DOI: https://doi.org/10.3350/cmh.2025.0125
  • 5,592 View
  • 26 Download

Editorial

Can SAFE score be utilized as a universal hepatocellular carcinoma prediction score?: Editorial on “High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated steatotic liver disease”
Michael Kwan-Lung Ko, Loey Lung-Yi Mak
Clin Mol Hepatol 2026;32(1):371-373.
Published online February 11, 2025
DOI: https://doi.org/10.3350/cmh.2025.0118

Citations

Citations to this article as recorded by  Crossref logo
  • HCC predictors in routine practice for patients with chronic liver diseases: Correspondence to editorial on “High SAFE scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction associated steatotic liver disease”
    Tung-Hung Su, Jia-Horng Kao
    Clinical and Molecular Hepatology.2026; 32(1): e52.     CrossRef
  • Correspondence to editorial 1 on “Baveno VI-SSM stratifies the risk of portal hypertension-related events in patients with HBV-related cirrhosis”
    Haiyu Wang, Jinjun Chen
    Clinical and Molecular Hepatology.2026; 32(1): e58.     CrossRef
  • 4,335 View
  • 43 Download
  • Crossref

Correspondence

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
Clin Mol Hepatol 2025;31(2):e173-e175.
Published online January 9, 2025
DOI: https://doi.org/10.3350/cmh.2025.0001

Citations

Citations to this article as recorded by  Crossref logo
  • 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
  • 5,941 View
  • 32 Download
  • 1 Web of Science
  • Crossref

Letters to the Editor

Current burden of MASLD, MetALD, and hepatic fibrosis among US adults with prediabetes and diabetes, 2017–2023
Donghee Kim, Rohit Loomba, Aijaz Ahmed
Clin Mol Hepatol 2025;31(3):e235-e238.
Published online December 30, 2024
DOI: https://doi.org/10.3350/cmh.2024.1150

Citations

Citations to this article as recorded by  Crossref logo
  • Association of gut microbiota dietary index with metabolic dysfunction-associated steatotic liver disease: the mediating roles of inflammation and body mass index
    Yu Pu, Zongbiao Tan, Yanrui Wu, Suqi Zeng, Haodong He, Jixiang Zhang, Weiguo Dong
    Frontiers in Nutrition.2025;[Epub]     CrossRef
  • Advances in identifying risk factors of metabolic dysfunction-associated alcohol-related liver disease
    Rui-Qi Ye, Yi-Fan Chen, Chang Ma, Xi Cheng, Wei Guo, Sha Li
    Biomedicine & Pharmacotherapy.2025; 188: 118191.     CrossRef
  • Disproportionately rising mortality rates of alcohol-associated acute Pancreatitis: Analysis from centers for Disease Control and prevention database (2011–2020)
    Pojsakorn Danpanichkul, Yanfang Pang, Donghee Kim, Thanida Auttapracha, Shu-Yen Chan, Do Han Kim, Thanawin Pramotedham, Kanita Mankan, Chanokporn Puchongmart, Juan Pablo Arab, Luis Antonio Diaz, Jorge D. Machicado, Michael B. Wallace, Karn Wijarnpreecha
    Pancreatology.2025; 25(4): 508.     CrossRef
  • A Comparison of the Predictive Value of 12 Body Composition Markers for Metabolic Dysfunction-Associated Steatotic Liver Disease, At-Risk Metabolic Dysfunction-Associated Steatohepatitis, and Increased Liver Stiffness in a General Population Setting
    Laurens A. van Kleef, Maurice Michel, Mesut Savas, Jesse Pustjens, Roel van de Laar, Edith Koehler, Elisabeth F.C. van Rossum, Harry L.A. Janssen, Jörn M. Schattenberg, Willem P. Brouwer
    American Journal of Gastroenterology.2025;[Epub]     CrossRef
  • Extrahepatic manifestation of metabolic dysfunction-associated steatotic liver disease
    Anoushka Shenoy, Aijaz Ahmed, Donghee Kim
    Metabolism and Target Organ Damage.2025;[Epub]     CrossRef
  • Organokine-Mediated Crosstalk: A Systems Biology Perspective on the Pathogenesis of MASLD—A Narrative Review
    Sandra Maria Barbalho, Lucas Fornari Laurindo, Vitor Engracia Valenti, Nahum Méndez-Sánchez, Mariana M. Ramírez-Mejía, Ricardo de Alvares Goulart
    International Journal of Molecular Sciences.2025; 26(23): 11547.     CrossRef
  • Editorial: Understanding How Social Determinants of Health Impact Mortality in MASLD—Insights From a National Analysis. Authors' Reply
    Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Rohit Loomba, Aijaz Ahmed
    Alimentary Pharmacology & Therapeutics.2025;[Epub]     CrossRef
  • 10,122 View
  • 231 Download
  • 4 Web of Science
  • Crossref

Steatotic liver disease

MAFLD or MASLD: Which better represents the prognosis of the steatotic liver population: Letter to the editor on “Evolutionary changes in metabolic dysfunction-associated steatotic liver disease and risk of hepatocellular carcinoma: A nationwide cohort study”
Ying Wang, Shengfeng Wang, Xiude Fan, Jiajun Zhao, Yongfeng Song
Clin Mol Hepatol 2025;31(2):e128-e133.
Published online December 26, 2024
DOI: https://doi.org/10.3350/cmh.2024.1008

Citations

Citations to this article as recorded by  Crossref logo
  • Associations between systemic inflammatory biomarkers and metabolic dysfunction associated steatotic liver disease: a cross-sectional study of NHANES 2017–2020
    Xin Qiu, Shuang Shen, Nizhen Jiang, Yifei Feng, Guodong Yang, Donghong Lu
    BMC Gastroenterology.2025;[Epub]     CrossRef
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    Seogsong Jeong, Won Kim, Sang Min Park
    Clinical and Molecular Hepatology.2025; 31(2): e210.     CrossRef
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Original Articles

Artificial intelligence, epidemiology, methodology, or others

Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta-oxidation
Ester Ciociola, Tanmoy Dutta, Kavitha Sasidharan, Lohitesh Kovooru, Francesca R. Noto, Grazia Pennisi, Salvatore Petta, Angela Mirarchi, Samantha Maurotti, Bernardette Scopacasa, Luca Tirinato, Patrizio Candeloro, Marcus Henricsson, Daniel Lindén, Oveis Jamialahmadi, Arturo Pujia, Rosellina M. Mancina, Stefano Romeo
Clin Mol Hepatol 2025;31(2):445-459.
Published online December 23, 2024
DOI: https://doi.org/10.3350/cmh.2024.0642
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global epidemic. The disease has a strong genetic component, and a common missense variant (rs2642438) in the mitochondrial amidoxime-reducing component 1 (MARC1) gene confers protection against its onset and severity. However, there are contrasting results regarding the mechanisms that promote this protection.
Methods
We downregulated MARC1 in primary human hepatocytes (PHHs) using short interfering RNA (siRNA). We measured neutral lipid content by Oil-Red O staining and fatty acid oxidation by radiolabeled tracers. We also performed RNA-sequencing and proteomic analysis using LC-MS. Additionally, we analyzed data from 239,075 participants from the UK Biobank.
Results
Downregulation of MARC1 reduced neutral lipid content in PHHs homozygous for the wild type (p.A165, risk), but not for the mutant (p.T165, protective), allele. We found that this reduction was mediated by increased fatty acid utilization via β-oxidation. Consistent with these results, we found that the levels of 3-hydroxybutyrate, a by-product of β-oxidation, were higher in carriers of the rs2642438 minor allele among samples from the UK biobank, indicating higher β-oxidation in these individuals. Moreover, downregulation of the MARC1 p.A165 variant resulted in a more favorable phenotype by reducing ferroptosis and reactive oxygen species levels.
Conclusions
MARC1 downregulation in carriers of the risk allele results in lower hepatocyte neutral lipids content due to higher β-oxidation, while upregulating beneficial pathways involved in cell survival.

Citations

Citations to this article as recorded by  Crossref logo
  • Loss of Mtarc1 Protects Against Steatotic Liver Disease in Mice
    Xiaofei Yin, Caroline Bickerton, Bryan MacDonald, Alessandro Arduini, Yunlong Shi, Mary Haas, Amy Deik, Mark Chaffin, Erika Kovacs‐Bogdan, Julian Avila Pacheco, Maiwen Amegadjie, Bidur Bhandary, Shayan Sadre, Thomas Rathjen, Irinna Papangeli, Raymond T. C
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    Frontiers in Microbiology.2026;[Epub]     CrossRef
  • Evolutionäre Aspekte der mit metabolischer Dysfunktion assoziierten steatotischen Lebererkrankung (MASLD)
    Andreas Geier, Stephan Schiffels, Marcin Krawczyk
    Die Gastroenterologie.2025; 20(2): 94.     CrossRef
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  • Crossref

Steatotic liver disease

Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
Clin Mol Hepatol 2025;31(2):382-393.
Published online November 29, 2024
DOI: https://doi.org/10.3350/cmh.2024.0987
Background/Aims
Multi-society experts proposed the adoption of new terminology, metabolic dysfunctionassociated steatotic liver disease (MASLD) and steatotic liver disease (SLD). We studied the current prevalence of SLD and its subcategories in the US.
Methods
Using the recent National Health and Nutrition Examination Survey from 2017 to 2023, we analyzed data from 12,199 participants (≥18 years) who completed transient elastography. SLD and its subcategories, including MASLD, metabolic and alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD), were categorized according to consensus nomenclature.
Results
The age-adjusted prevalence of SLD (cut-off: 285 dB/m) was 35.0% (95% confidence interval [CI] 33.4–36.7). Within this category, the age-adjusted prevalence for MASLD was 31.9% (95% CI 30.4–33.4), MetALD 2.2% (95% CI 1.8–2.6), and ALD 0.8% (95% CI 0.6–1.1). The prevalence of SLD and MASLD showed a statistically insignificant decrease during COVID-19, while ALD increased without significance. In contrast, the prevalence of advanced fibrosis in SLD was significantly higher during the COVID-19 era, at 9.8% for 285 dB/m and 7.8% for 263 dB/m, compared to 7.4% (P=0.039) and 6% (P=0.041) in the pre-COVID-19 era. The proportion of advanced fibrosis and cirrhosis in individuals with ALD was two-fold higher than MASLD and MetALD, largely due to increases during the COVID-19 era.
Conclusions
While the prevalence of SLD and its subcategories remained stable, there was a significant increase in advanced fibrosis among SLD individuals during the COVID-19 era, with ALD having a proportion of advanced fibrosis and cirrhosis that was twice as high as MASLD and MetALD.

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    Pojsakorn Danpanichkul, Kwanjit Duangsonk, Claire S. Faulkner, Supapitch Sirimangklanurak, Tulaton Sodsri, Natchaya Polpichai, Shu-Yen Chan, Yanfang Pang, Omar Y. Mousa, Donghee Kim, Suthat Liangpunsakul, Karn Wijarnpreecha
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Review

Steatotic liver disease

Long-term outcomes and risk modifiers of metabolic dysfunction-associated steatotic liver disease between lean and non-lean populations
Pojsakorn Danpanichkul, Kanokphong Suparan, Vitchapong Prasitsumrit, Aijaz Ahmed, Karn Wijarnpreecha, Donghee Kim
Clin Mol Hepatol 2025;31(1):74-89.
Published online October 23, 2024
DOI: https://doi.org/10.3350/cmh.2024.0631
One-third of adults across the globe exhibit metabolic dysfunction-associated steatotic liver disease (MASLD)―formerly known as nonalcoholic fatty liver disease (NAFLD). To date, MASLD is the fastest-growing etiology of chronic liver disease and hepatocellular carcinoma (HCC). Besides the population with obesity, MASLD can also be found in lean populations, accounting for 13% of the global population, especially Asians. Notably, individuals with lean MASLD face equal or higher overall mortality rates compared to their non-lean counterparts. Risk modifiers encompass advanced age, hepatic fibrosis, and type 2 diabetes mellitus (T2DM). Moreover, the population with lean MASLD is associated with an increased risk of HCC, while their non-lean counterparts are more prone to cardiovascular outcomes and T2DM. Existing evidence indicates a similar risk of liver-related events and extrahepatic cancer between the two groups. However, MASLD-related genetic variants, such as PNPLA3 and TM6SF2, did not significantly affect mortality between the two populations. Still, underreporting alcohol consumption and regional representation limits the study’s comprehensiveness. Longitudinal studies and mechanistic explorations are needed to understand differences in lean versus non-lean MASLD populations. This review highlights the need for awareness and tailored interventions in managing MASLD, considering lean individuals’ unique risks.

Citations

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  • Dietary vitamin E intake in metabolic dysfunction–associated steatotic liver disease and all-cause/cause-specific mortality
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    Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
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    Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Rohit Loomba, Aijaz Ahmed
    Clinical and Molecular Hepatology.2025; 31(2): e180.     CrossRef
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    Donghyun Ko, Do Han Kim, Pojsakorn Danpanichkul, Masahito Nakano, Chitchai Rattananukrom, Karn Wijarnpreecha, Cheng Han Ng, Mark D Muthiah
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  • Increased Mortality Among Lean Versus Non‐Lean Adults With MASLD: A Multicenter Study
    Leith Ghani, Majd B. Aboona, Claire S. Faulkner, Pooja Rangan, Moises Nevah Rubin, Ma Ai Thanda Han, Michael B. Fallon, Vincent L. Chen, Karn Wijarnpreecha
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    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
    Journal of Gastroenterology and Hepatology.2025; 40(8): 2053.     CrossRef
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    Matthew Kubina, Vitchapong Prasitsumrit, Jarell Tan, Joo Wei Ethan Quek, Dhiraj Peddu, Ankit Mishra, Pojsakorn Danpanichkul, Jake P. Mann, Eric Trépo, Stephan Buch, Daniel Q. Huang, Cheng Han Ng, Mark D. Muthiah, Yu Jun Wong, Karn Wijarnpreecha, Vincent L
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    Eva Juárez-Hernández, Montserrat Berrospe-Alfaro, Misael Uribe, Iván López-Mendez
    Journal of Clinical and Experimental Hepatology.2025; 15(6): 103114.     CrossRef
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    Donghee Kim, Rohit Loomba, Aijaz Ahmed
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    Frontiers in Endocrinology.2025;[Epub]     CrossRef
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    Alcohol, Clinical and Experimental Research.2025; 49(11): 2451.     CrossRef
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    Ming-Ling Chang, Jur-Shan Cheng, Jennifer Tai, Wei-Ting Chen, Sien-Sing Yang, Cheng-Hsun Chiu, Rong-Nan Chien, Chia-Lin Hsu, Shang-Jung Wu, Cathy SJ Fann
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    Zhenyu Huo, Yijun Chen, Yating Huang, Zhirong Yang, Yujun Long, Qian Zhang, Shuohua Chen, Guodong Wang, Shengtao Zhu, Dianjianyi Sun, Canqing Yu, Jun Lv, Liming Li, Ming-Hua Zheng, Shouling Wu, Yuanjie Pang, Shanshan Wu
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    Gerard Stupecki, Emilia Kowalczyk, Agnieszka Ciba-Stemplewska, Magdalena Dolecka-Ślusarczyk, Iwona Gorczyca-Głowacka
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    Karina Mireya Palacios Girón, Zamira Helena Hernandez Nazara, Montserrat Maldonado-González, Erika Martínez-López, Martha P. Sánchez Muñoz, Carlos Alfredo Bautista López, Ma. Soledad Aldana Aguiñaga, Jose Alfredo Dominguez-Rosales, Belinda Vargas-Guerrero
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  • Implication of the Androgen Receptor in Muscle–Liver Crosstalk: An Overlooked Mechanistic Link in Lean-MASLD
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    Livers.2025; 5(4): 65.     CrossRef
  • Intestinal NLRP3 Deficiency Exacerbates MASLD in Male Mice via Reduced Butyrate Production
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    Mohammed Rifat Shaik, Yaron Rotman
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Original Article

Steatotic liver disease

Metabolic dysfunction-associated steatotic liver disease exhibits sex-specific microbial heterogeneity within intestinal compartments
Carlos Jose Pirola, Maria Silvina Landa, Mariano Schuman, Silvia Inés García, Adrian Salatino, Silvia Sookoian
Clin Mol Hepatol 2025;31(1):179-195.
Published online October 11, 2024
DOI: https://doi.org/10.3350/cmh.2024.0359
Background/Aims
Evidence suggests that the gastrointestinal microbiome plays a significant role in the biology of metabolic dysfunction-associated steatotic liver disease (MASLD). However, it remains unclear whether disparities in the gut microbiome across intestinal tissular compartments between the sexes lead to MASLD pathogenesis.
Methods
Sex-specific analyses of microbiome composition in two anatomically distinct regions of the gut, the small intestine and colon, were performed using an experimental model of MASLD. The study involved male and female spontaneously hypertensive rats and the Wistar-Kyoto control rat strain, which were fed either a standard chow diet or a high-fat diet for 12 weeks to induce MASLD (12 rats per group). High-throughput 16S sequencing was used for microbiome analysis.
Results
There were significant differences in the overall microbiome composition of male and female rats with MASLD, including variations in topographical gut regions. The beta diversity of the jejunal and colon microbiomes was higher in female rats than in male rats (PERMANOVA p-value=0.001). Sex-specific analysis and discriminant features using LEfSe showed considerable variation in bacterial abundance, along with distinct functional properties, in the jejunum and colon of animals with MASLD. Significantly elevated levels of lipopolysaccharide and protein expression of Toll-like receptor 4 were observed in the livers of male rats with MASLD compared with their female counterparts.
Conclusions
This study uncovered sexual dimorphism in the gut microbiome of MASLD and identified microbial heterogeneity within intestinal compartments. Insights into sex-specific variations in gut microbiome composition could facilitate customised treatment strategies.

Citations

Citations to this article as recorded by  Crossref logo
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    Massimo De Luca, Rita Verdoliva, Anna Lombardi, Antonio Giorgio
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    Bryan Adrian Priego-Parra, Berenice M Román-Calleja, Rocio Gallego-Duran, Jordi Gracia-Sancho, Jose Antonio Velarde Ruiz-Velasco, Jose Maria Remes-Troche
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Correspondences

Steatotic liver disease

Correspondence to letter to the editor on “Bariatric intervention improves metabolic dysfunction-associated steatohepatitis in patients with obesity: A systematic review and meta-analysis”
Yuri Cho, Dae Won Jun
Clin Mol Hepatol 2025;31(1):e103-e104.
Published online September 24, 2024
DOI: https://doi.org/10.3350/cmh.2024.0818
  • 4,305 View
  • 46 Download

Steatotic liver disease

Correspondence to editorial on “DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease”
Amal Magdy, Hee-Jin Kim, Won Kim, Mirang Kim
Clin Mol Hepatol 2025;31(1):e70-e73.
Published online September 10, 2024
DOI: https://doi.org/10.3350/cmh.2024.0761
  • 4,368 View
  • 86 Download

Editorials

Steatotic liver disease

A complement to epigenetics in metabolic dysfunction-associated steatotic liver disease: Editorial on “DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease”
Johanna K. DiStefano, Glenn S. Gerhard
Clin Mol Hepatol 2025;31(1):297-300.
Published online August 27, 2024
DOI: https://doi.org/10.3350/cmh.2024.0704

Citations

Citations to this article as recorded by  Crossref logo
  • Correspondence to editorial on “DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease”
    Amal Magdy, Hee-Jin Kim, Won Kim, Mirang Kim
    Clinical and Molecular Hepatology.2025; 31(1): e70.     CrossRef
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  • Crossref

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
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    Personalized Medicine.2025; 22(2): 113.     CrossRef
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    Trends in Endocrinology & Metabolism.2025; 36(11): 1000.     CrossRef
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  • Crossref

Letter to the Editor

Steatotic liver disease

Leukocyte telomere shortening in metabolic dysfunction-associated steatotic liver disease and all-cause/cause-specific mortality
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
Clin Mol Hepatol 2024;30(4):982-986.
Published online August 27, 2024
DOI: https://doi.org/10.3350/cmh.2024.0691

Citations

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  • Telomere length and metabolic dysfunction-associated steatotic liver disease risk and progression: A systematic review and meta-analysis
    Chunfeng Sun, Ping Qiu, Shuo Huang, Qihan Luo, Qing Ma, Piao Hu, Fangming Chen, Hongyan Wu, Chunxiao Chen
    Experimental Gerontology.2026; 214: 113036.     CrossRef
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Correspondence

Viral hepatitis

Steatotic liver disease in chronic hepatitis C related hepatocellular carcinoma: Inflictor or bystander?: Correspondence to editorial on “Dynamic change of metabolic dysfunction-associated steatotic liver disease in chronic hepatitis C patients after viral eradication: A nationwide registry study in Taiwan”
Chung-Feng Huang, Ming-Lun Yeh, Chia-Yen Dai, Jee-Fu Huang, Wan-Long Chuang, Ming-Lung Yu
Clin Mol Hepatol 2025;31(1):e64-e66.
Published online August 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0638

Citations

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  • Hepatocellular carcinoma surveillance after sustained virological response in chronic hepatitis C: Editorial on “Non-invasive prediction of post-sustained virological response hepatocellular carcinoma in hepatitis C virus: A systematic review and meta-ana
    Ho Soo Chun, Minjong Lee
    Clinical and Molecular Hepatology.2025; 31(1): 261.     CrossRef
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Review

Steatotic liver disease

Epidemiology of metabolic dysfunction-associated steatotic liver disease
Zobair M. Younossi, Markos Kalligeros, Linda Henry
Clin Mol Hepatol 2025;31(Suppl):S32-S50.
Published online August 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0431
As the rates of obesity and type 2 diabetes (T2D) continue to increase globally, so does the prevalence of metabolic dysfunction–associated steatotic liver disease (MASLD). Currently, 38% of all adults and 7–14% of children and adolescents have MASLD. By 2040, the MASLD prevalence rate for adults is projected to increase to more than 55%. Although MASLD does not always develop into progressive liver disease, it has become the top indication for liver transplant in the United States for women and those with hepatocellular carcinoma (HCC). Nonetheless, the most common cause of mortality among patients with MASLD remains cardiovascular disease. In addition to liver outcomes (cirrhosis and HCC), MASLD is associated with an increased risk of developing de novo T2D, chronic kidney disease, sarcopenia, and extrahepatic cancers. Furthermore, MASLD is associated with decreased health-related quality of life, decreased work productivity, fatigue, increased healthcare resource utilization, and a substantial economic burden. Similar to other metabolic diseases, lifestyle interventions such as a heathy diet and increased physical activity remain the cornerstone of managing these patients. Although several obesity and T2D drugs are available to treat co-morbid disease, resmetirom is the only MASH-targeted medication for patients with stage 2–3 fibrosis that has approved by the Food and Drug Administration for use in the United States. This review discusses MASLD epidemiology and its related risk factors and outcomes and demonstrates that without further global initiatives, MASLD incidence could continue to increase.

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  • The burden and mortality impact of cardiovascular disease–metabolic dysfunction–associated steatotic liver disease comorbidity
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  • Kefiran, a polysaccharide from kefir grain, modulates gut microbiota and hepatic metabolism to mitigate metabolic dysfunction-associated steatotic liver disease
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  • Assessment of the Diagnostic Performance and Clinical Impact of AI in Hepatic Steatosis: Systematic Review and Meta-Analysis
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  • Multi-Omics Evidence Linking Depression to MASLD Risk via Inflammatory Immune Signaling
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  • Diet intervention altered DNA methylation of potassium voltage-gated channel subfamily Q member 1 in metabolic dysfunction-associated steatohepatitis
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  • Artificial Intelligence for Fibrosis Diagnosis in Metabolic-Dysfunction-Associated Steatotic Liver Disease: A Systematic Review
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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
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  • Use of Artificial Intelligence-Assisted Histopathology for Evaluation of Sex-Specific Progression and Regression of Hepatocellular Carcinoma Related to Metabolic Dysfunction-Associated Fatty Liver Disease
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  • Phosphatidylserine Supplementation Improves Metabolic Liver Disease and Glycemic Control in the Presence of Suppressed Oxidative Glucose Metabolism
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  • Integrating multi-omics and machine learning systematically deciphers cellular heterogeneity and fibrotic regulatory networks in the progression from MASLD to MASH
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  • High-Intensity Interval Training Reduces Liver Enzyme Levels and Improves MASLD-Related Biomarkers in Overweight/Obese Girls
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  • Association of high-sensitivity C-reactive protein with hepatic fibrosis in patients with metabolic dysfunction-associated steatotic liver disease
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  • Lean MASLD and IBD: Exploring the Intersection of Metabolic Dysfunction and the Gut–Liver Axis
    Adrian Rotaru, Remus Stafie, Ermina Stratina, Sebastian Zenovia, Robert Nastasa, Horia Minea, Laura Huiban, Tudor Cuciureanu, Cristina Muzica, Stefan Chiriac, Irina Girleanu, Ana-Maria Singeap, Catalin Sfarti, Carol Stanciu, Anca Trifan
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  • Sex differences in diet-induced MASLD – are female mice naturally protected?
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    Tsubasa Tsutsumi, Takumi Kawaguchi, Hideki Fujii, Yoshihiro Kamada, Yuichiro Suzuki, Koji Sawada, Miwa Tatsuta, Tatsuji Maeshiro, Hiroshi Tobita, Takemi Akahane, Chitomi Hasebe, Miwa Kawanaka, Takaomi Kessoku, Yuichiro Eguchi, Hayashi Syokita, Atsushi Nak
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  • Association of High‐Sensitivity Troponins in Metabolic Dysfunction‐Associated Steatotic Liver Disease With All‐Cause and Cause‐Specific Mortality
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    Metabolism.2025; 168: 156253.     CrossRef
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  • Significance of FXR agonists in MASLD treatment: a deep dive into lipid alteration by analytical techniques
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    Alimentary Pharmacology & Therapeutics.2025; 61(9): 1565.     CrossRef
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    Trends in Endocrinology & Metabolism.2025; 36(11): 1000.     CrossRef
  • Use of Hepatoscope 2DTE for non-invasive assessment of liver stiffness among Mexican immigrant adults in a community-based setting
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    Clinics and Research in Hepatology and Gastroenterology.2025; 49(5): 102581.     CrossRef
  • Potential bidirectional communication between the liver and the central circadian clock in MASLD
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  • GOLM1 and bile acid synthesis: Correspondence to editorial on “GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers”
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    Clinical and Molecular Hepatology.2025; 31(2): e189.     CrossRef
  • Prevalence of steatotic liver disease and associated fibrosis in the general population: An epidemiological survey: Letter to the editor on “Epidemiology of metabolic dysfunction-associated steatotic liver disease”
    Lin Guan, Xinhe Zhang, Shanghao Liu, Xiaolong Qi, Yiling Li
    Clinical and Molecular Hepatology.2025; 31(2): e145.     CrossRef
  • Prognostic impact of body composition in hepatocellular carcinoma patients undergoing interventional and systemic therapy
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    Liver International.2025;[Epub]     CrossRef
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  • Multi‐Center, Multi‐Vendor Validation of Simultaneous MRI‐Based Proton Density Fat Fraction and R2* Mapping Using a Combined Proton Density Fat Fraction‐R2* Phantom
    Jitka Starekova, David Rutkowski, Won C. Bae, Hung Do, Ananth J. Madhuranthakam, Vadim Malis, Sheng Qing Lin, Suraj Serai, Takeshi Yokoo, Scott B. Reeder, Jean H. Brittain, Diego Hernando
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  • Overcoming barriers to unlock the therapeutic potential of saroglitazar for the management of metabolic dysfunction-associated steatotic liver disease
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    Clinical Nutrition.2025; 49: 52.     CrossRef
  • Targeting Metabolism: Innovative Therapies for MASLD Unveiled
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    International Journal of Molecular Sciences.2025; 26(9): 4077.     CrossRef
  • Psoriasis, metabolic syndrome and methotrexate: Is this association suitable for a new subcategory in steatotic liver disease?
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  • Evaluating the RESET care program: Advancing towards scalable and effective healthcare solutions for metabolic dysfunction-associated liver disease
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  • Association between glucose time-in-range and the severity of metabolic dysfunction-associated steatotic liver disease in Chinese adults with type 2 diabetes mellitus
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  • Association between dietary amino acid intake and the risk of metabolic dysfunction-associated steatotic liver disease
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  • Low carbohydrate and low-calorie diets reduce liver fat and lower brain glutamate and myo-inositol levels in patients with Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
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  • FGF21 reverses MASH through coordinated actions on the CNS and liver
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    Donghyun Ko, Do Han Kim, Pojsakorn Danpanichkul, Masahito Nakano, Chitchai Rattananukrom, Karn Wijarnpreecha, Cheng Han Ng, Mark D Muthiah
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  • Prevalence of MASLD, Met-ALD, and ALD and Associated Fibrosis Among US Adults
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  • Association between weight fluctuation and the risk of metabolic dysfunction-associated steatotic liver disease
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    Current Medical Research and Opinion.2025; 41(11): 2089.     CrossRef
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    Sina Bazmi, Mohammadreza Fardaei, Reza Homayounfar, Maryam Kazemi, Babak Pezeshki, Reza Malekzadeh, Nasrollah Ghahramani, Mojtaba Farjam
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    Constantine N. Tzouanas, Jessica E.S. Shay, Marc S. Sherman, Adam J. Rubin, Benjamin E. Mead, Tyler T. Dao, Junyan Tao, Brandon M. Lehrich, George Eng, Jeffrey Patterson-Fortin, Titus Butzlaff, Miyeko D. Mana, Kellie E. Kolb, Chad Walesky, Brian J. Pepe-M
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    Jian-Jun Lou, Jing Zeng
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    Diabetes Therapy.2025;[Epub]     CrossRef
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    Bruno Basil, Winifred Adiri, Ejike Lawrence Ugwu, Ngozi Ijeoma Okoro
    Diabetology & Metabolic Syndrome.2025;[Epub]     CrossRef
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    Xiaoping Liu, Ping Yuan, Ying Huang
    European Journal of Medical Research.2025;[Epub]     CrossRef
  • Associations Between Systemic Inflammatory Markers, Metabolic Dysfunction, and Liver Fibrosis Scores in Patients with MASLD
    Ragaey Ahmad Eid, Ahmed Moheyeldien Hamed, Sara O. Elgendy, Khalid M. Orayj, Ahmed R. N. Ibrahim, Ahmed M. Abdel Hamied, Engy A. Wahsh, Maha Youssif, Hoda Rabea, Yasmin M. Madney, Dina Attia, Shaymaa Nafady
    Metabolites.2025; 16(1): 25.     CrossRef
  • Phase III, multicenter, randomized, double-blind, placebo-controlled study of norursodeoxycholic acid in metabolic dysfunction-associated steatotic liver disease patients
    Veerendra Kumar Panuganti, Chandrasekhar Varma Alluri, Javeed Mohammad, Mamatha Reddy Dundigalla, Pavan Kumar Madala, Sanyasirao KSSVV, Althaf Shaik
    World Journal of Hepatology.2025;[Epub]     CrossRef
  • Interplay between intestinal permeability and metabolic dysfunction-associated steatotic liver disease: Could there be a role for extra virgin olive oil consumption?
    Lydia Giannitrapani, Marinella Ferraro, Aurelio Seidita, Anna Licata, Maurizio Soresi
    World Journal of Hepatology.2025;[Epub]     CrossRef
  • Does Continuous Positive Airway Pressure Improve Liver Outcomes in MASLD with Obstructive Sleep Apnea? A Systematic Review
    Theja V. Channapragada, Clinton R. Brenner, Keven Guruswamy, Rewanth Katamreddy, Alwyn T. Pandian, Vyshnavi Pendala, Jaydon J. Sam, Jonathan G. Stine, Michael J. Brenner, Vinciya Pandian
    Journal of Clinical Medicine.2025; 15(1): 225.     CrossRef
  • Independent and Combined Effects of Resistance Training and Whey Protein on Skeletal Muscle Mass and Function in Individuals with MASLD Under Caloric Restriction
    Chae-Been Kim, Jinwoo Sung, Dohyun Ahn, Eun-Ah Jo, Kyung-Wan Baek, Hae-Ri Heo, Ju-Hwan Oh, Fengrui Zhang, Hyoung-Su Park, Hong-Soo Kim, Jung-Jun Park
    Nutrients.2025; 18(1): 83.     CrossRef
  • SGLT2 Inhibitors as Systemic Metabolic Modulators: Linking Glucose Excretion to Liver Function Restoration
    Seung Wan Noh, Han Sol Ryu, Yong-Ho Kim, Byung-Chul Oh
    Endocrinology and Metabolism.2025; 40(6): 851.     CrossRef
  • Impact of liraglutide and dapagliflozin on steatosis, fibrosis, aminotransferases, and lipid profile in patients with metabolic dysfunction-associated steatotic liver disease and type 2 diabetes mellitus: results of a 6-month randomized study
    V.V. Cherniavskyi, A.I. Akimov, V.V. Tishchenko, L.M. Parunian
    GASTROENTEROLOGY.2025; 59(4): 269.     CrossRef
  • Circulating histones as potential biomarkers of MASLD-MASH-HCC progression
    Desislava K. Tsoneva, Diana Buzova, Salvatore Daniele Bianco, Maria Rita Braghini, Giulia Andolina, Antonio Liguori, Francesca D’ Ambrosio, Andrea Urbani, Antonio Gasbarrini, Maurizio Pompili, Anna Alisi, Jan Cerveny, Tommaso Mazza, Manlio Vinciguerra, Lu
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    Gabriel dos Santos, Fabio de Castro Machado, Ana Beatriz Serrato Carmo, Alvaro Ivanski Sabedotti, Laura Moscardi Milléo, Lorenzo Cultz, Mateus Baptista Pizyblski, Leonardo Henrique de Figueiredo Lima, Mário Cláudio Soares Sturzeneker
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  • THE EFFECT OF S-ADENOSYLMETHIONINE ON LIPID PROFILE PARAMETERS IN PATIENTS WITH MULTIPLE MYELOMA AND CONCOMITANT METABOLIC DYSFUNCTION–ASSOCIATED STEATOTIC LIVER DISEASE DURING CHEMOTHERAPY
    Y. Stadnik, G. Maslova
    Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії.2025; 25(4): 76.     CrossRef
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    Zhengqi Wei, Jincheng Liu, Na Wang, Keke Wei
    Environmental Research.2024; 263: 120092.     CrossRef
  • Assessing Mortality Disparities Among Non-Alcoholic Fatty Liver Disease Metabolic Dysfunction Fatty Liver Disease and Metabolic Dysfunction-Associated Liver Disease: A Comprehensive Meta-Analysis
    Fahad Lakhdhir, Agha Syed Muhammad, Ahmed Nasir Qureshi, Imran A Shaikh, Imran Joher, Jawaria Majeed, Javaria Khan
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    Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, George Cholankeril, Aijaz Ahmed
    Clinical and Molecular Hepatology.2024; 30(4): 982.     CrossRef
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    Han Ah Lee
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Letter to the Editor

Steatotic liver disease

Differences in major adverse cardiovascular events of metabolic dysfunction-associated steatotic liver disease by race and ethnicity: Letter to the editor on “Differences in liver and mortality outcomes of non-alcoholic fatty liver disease by race and ethnicity: A longitudinal real-world study”
Hui-Chin Chang, Wen-Chieh Liao, Yi-Jen Fang, Shiu-Jau Chen, Shuo-Yan Gau
Clin Mol Hepatol 2024;30(4):978-981.
Published online August 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0565

Citations

Citations to this article as recorded by  Crossref logo
  • Small intestinal bacterial overgrowth and metabolic dysfunction-associated steatotic liver disease
    Ziteng Wang, Wentao Tan, Jiali Huang, Qian Li, Jing Wang, Hui Su, Chunmei Guo, Hong Liu
    Frontiers in Nutrition.2024;[Epub]     CrossRef
  • Comparisons of Post-Load Glucose at Different Time Points for Identifying High Risks of MASLD Progression
    Long Teng, Ling Luo, Yanhong Sun, Wei Wang, Zhi Dong, Xiaopei Cao, Junzhao Ye, Bihui Zhong
    Nutrients.2024; 17(1): 152.     CrossRef
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  • Crossref

Snapshot

Steatotic liver disease

Metabolic dysfunction-associated steatotic liver disease across women’s reproductive lifespan and issues
Clara Meda, Arianna Dolce, Sara Della Torre
Clin Mol Hepatol 2025;31(1):327-332.
Published online August 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0419

Citations

Citations to this article as recorded by  Crossref logo
  • Biological determinants and outcomes of sex discrepancies in MASLD
    Amedeo Lonardo, Mohamad Jamalinia, Ralf Weiskirchen
    Metabolism and Target Organ Damage.2026;[Epub]     CrossRef
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    Ralf Weiskirchen, Amedeo Lonardo
    International Journal of Molecular Sciences.2025; 26(13): 6382.     CrossRef
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    Ralf Weiskirchen, Amedeo Lonardo
    International Journal of Molecular Sciences.2025; 26(19): 9594.     CrossRef
  • Animal models of lean metabolic dysfunction-associated steatotic liver disease (MASLD): bridging pathogenesis and novel drug discovery
    Stavros P. Papadakos, Chara Georgiadou, Eva Kassi, Rallia-Iliana Velliou, Antonios Chatzigeorgiou
    Expert Opinion on Drug Discovery.2025; 20(12): 1683.     CrossRef
  • Posicionamento sobre a Saúde Cardiometabólica ao Longo do Ciclo de Vida da Mulher – 2025
    Gláucia Maria Moraes de Oliveira, Maria Cristina Costa de Almeida, Cynthia Melissa Valério, Fernando Giuffrida, Larissa Espíndola Neto, Maria Cristina de Oliveira Izar, Celi Marques-Santos, Claudia Maria Vilas Freire, Carlos Japhet da Matta Albuquerque, A
    Arquivos Brasileiros de Cardiologia.2025;[Epub]     CrossRef
  • Position Statement on Cardiometabolic Health Across the Woman's Life Course – 2025
    Gláucia Maria Moraes de Oliveira, Maria Cristina Costa de Almeida, Cynthia Melissa Valério, Fernando Giuffrida, Larissa Espíndola Neto, Maria Cristina de Oliveira Izar, Celi Marques-Santos, Claudia Maria Vilas Freire, Carlos Japhet da Matta Albuquerque, A
    Arquivos Brasileiros de Cardiologia.2025;[Epub]     CrossRef
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    Young Mi Jung, Taesu Kim, Min-Jeong Oh, Dong Hyeon Lee, Geum Joon Cho, Won Kim
    Hepatology International.2025;[Epub]     CrossRef
  • Position Statement on Cardiometabolic Health Across the Woman's Life Course – 2025
    Gláucia Maria Moraes de Oliveira, Maria Cristina Costa de Almeida, Cynthia Melissa Valério, Fernando Giuffrida, Larissa Neto Espíndola, Maria Cristina de Oliveira Izar, Celi Marques-Santos, Claudia Maria Vilas Freire, Carlos Japhet da Matta Albuquerque, A
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  • Sex and gender differences in MASLD: pathophysiological mechanisms, clinical implications, and future directions
    Mohamad Jamalinia, Samira Saeian, Nima Nikkhoo, Amirhossein Nazerian, Kamran Bagheri Lankarani
    Metabolism and Target Organ Damage.2025;[Epub]     CrossRef
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    Jie Liao, Tingting Liu, Biao Huang, Xin Li, Aijie Xie, Hengxi Chen
    BMC Women's Health.2025;[Epub]     CrossRef
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Original Articles

Steatotic liver disease

Dynamic change of metabolic dysfunction-associated steatotic liver disease in chronic hepatitis C patients after viral eradication: A nationwide registry study in Taiwan
Chung-Feng Huang, Chia-Yen Dai, Yi-Hung Lin, Chih-Wen Wang, Tyng-Yuan Jang, Po-Cheng Liang, Tzu-Chun Lin, Pei-Chien Tsai, Yu-Ju Wei, Ming-Lun Yeh, Ming-Yen Hsieh, Chao-Kuan Huang, Jee-Fu Huang, Wan-Long Chuang, Ming-Lung Yu
Clin Mol Hepatol 2024;30(4):883-894.
Published online July 29, 2024
DOI: https://doi.org/10.3350/cmh.2024.0414
Background/Aims
Steatotic liver disease (SLD) is a common manifestation in chronic hepatitis C (CHC). Metabolic alterations in CHC are associated with metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to elucidate whether hepatitis C virus (HCV) eradication mitigates MASLD occurrence or resolution.
Methods
We enrolled 5,840 CHC patients whose HCV was eradicated by direct-acting antivirals in a nationwide HCV registry. MASLD and the associated cardiometabolic risk factors (CMRFs) were evaluated at baseline and 6 months after HCV cure.
Results
There were 2,147 (36.8%) patients with SLD, and 1,986 (34.0%) of them met the MASLD criteria before treatment. After treatment, HbA1c (6.0% vs. 5.9%, P<0.001) and BMI (24.8 kg/m2 vs. 24.7 kg/m2, P<0.001) decreased, whereas HDL-C (49.1 mg/dL vs. 51.9 mg/dL, P<0.001) and triglycerides (102.8 mg/dL vs. 111.9 mg/dL, P<0.001) increased significantly. The proportion of patients with SLD was 37.5% after HCV eradication, which did not change significantly compared with the pretreatment status. The percentage of the patients who had post-treatment MASLD was 34.8%, which did not differ significantly from the pretreatment status (P=0.17). Body mass index (BMI) (odds ratio [OR] 0.89; 95% confidence intervals [CI] 0.85–0.92; P<0.001) was the only factor associated with MASLD resolution. In contrast, unfavorable CMRFs, including BMI (OR 1.10; 95% CI 1.06–1.14; P<0.001) and HbA1c (OR 1.19; 95% CI 1.04–1.35; P=0.01), were independently associated with MASLD development after HCV cure.
Conclusions
HCV eradication mitigates MASLD in CHC patients. CMRF surveillance is mandatory for CHC patients with metabolic alterations, which are altered after HCV eradication and predict the evolution of MASLD.

Citations

Citations to this article as recorded by  Crossref logo
  • Editorial: Beyond Viral Eradication—Cardiometabolic Risk and Cardiovascular Outcomes After SVR in Chronic Hepatitis C. Authors' Reply
    Pei‐Chien Tsai, Jee‐Fu Huang, Ming‐Lung Yu
    Alimentary Pharmacology & Therapeutics.2026;[Epub]     CrossRef
  • Real‐world efficacy and safety of universal 8‐week glecaprevir/pibrentasvir in patients with chronic hepatitis C with early chronic kidney disease or pre‐end‐stage renal disease: Insights from a nationwide hepatisis C virus registry in Taiwan
    Szu‐Jen Wang, Chung‐Feng Huang, Te‐Sheng Chang, Ching‐Chu Lo, Chao‐Hung Hung, Chien‐Wei Huang, Lee‐Won Chong, Pin‐Nan Cheng, Ming‐Lun Yeh, Cheng‐Yuan Peng, Chien‐Yu Cheng, Jee‐Fu Huang, Ming‐Jong Bair, Chih‐Lang Lin, Chi‐Chieh Yang, Hsing‐Tao Kuo, Tsai‐Yu
    The Kaohsiung Journal of Medical Sciences.2025;[Epub]     CrossRef
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    Hung-Wei Wang, Cheng-Yuan Peng, Ming-Lung Yu
    Journal of the Formosan Medical Association.2025;[Epub]     CrossRef
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    Xia-Rong Liu, Szu-Ching Yin, Yi-Ting Chen, Mei-Hsuan Lee
    Journal of the Chinese Medical Association.2025; 88(5): 343.     CrossRef
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    Beom Kyung Kim
    Gut and Liver.2025; 19(5): 635.     CrossRef
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    Ana Virseda-Berdices, Belen Requena, Juan Berenguer, Juan Gónzalez-García, Carolina Gonzalez-Riano, Cristina Díez, Victor Hontañón, Paula Muñoz-García, Amanda Fernández-Rodríguez, Coral Barbas, Salvador Resino, Rubén Martín-Escolano, María Ángeles Jiménez
    Journal of Infection and Public Health.2025; 18(12): 102981.     CrossRef
  • Metabolic Dysfunction‐Associated Steatotic Liver Disease After Hepatitis C Virus Cure
    Chung‐Feng Huang, Jee‐Fu Huang, Ming‐Lung Yu, Wan‐Long Chuang
    The Kaohsiung Journal of Medical Sciences.2025;[Epub]     CrossRef
  • Advanced Fibrosis and Cardiometabolic Risk Burden Increase Major Cardiovascular Events in Chronic Hepatitis C Patients With Steatotic Liver Disease After Viral Eradication
    Pei‐Chien Tsai, Chung‐Feng Huang, Ming‐Lun Yeh, Yu‐Ju Wei, Chih‐Wen Wang, Tyng‐Yuan Jang, Po‐Cheng Liang, Yi‐Hung Lin, Chia‐Yen Dai, Jee‐Fu Huang, Wan‐Long Chuang, Ming‐Lung Yu
    Alimentary Pharmacology & Therapeutics.2025;[Epub]     CrossRef
  • Steatotic liver disease in patients with chronic hepatitis C
    Jakub Janczura, Michał Brzdęk, Robert Flisiak, Krystyna Dobrowolska, Kinga Brzdęk, Piotr Rzymski, Dorota Zarębska-Michaluk
    World Journal of Hepatology.2025;[Epub]     CrossRef
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  • 162 Download
  • 13 Web of Science
  • Crossref

Steatotic liver disease

DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease
Amal Magdy, Hee-Jin Kim, Hanyong Go, Jun Min Lee, Hyun Ahm Sohn, Keeok Haam, Hyo-Jung Jung, Jong-Lyul Park, Taekyeong Yoo, Eun-Soo Kwon, Dong Hyeon Lee, Murim Choi, Keon Wook Kang, Won Kim, Mirang Kim, on behalf of the Innovative Target Exploration of NAFLD (ITEN) Consortium
Clin Mol Hepatol 2024;30(4):824-844.
Published online July 25, 2024
DOI: https://doi.org/10.3350/cmh.2024.0229
Background/Aims
Blocking the complement system is a promising strategy to impede the progression of metabolic dysfunction–associated steatotic liver disease (MASLD). However, the interplay between complement and MASLD remains to be elucidated. This comprehensive approach aimed to investigate the potential association between complement dysregulation and the histological severity of MASLD.
Methods
Liver biopsy specimens were procured from a cohort comprising 106 Korean individuals, which included 31 controls, 17 with isolated steatosis, and 58 with metabolic dysfunction–associated steatohepatitis (MASH). Utilizing the Infinium Methylation EPIC array, thorough analysis of methylation alterations in 61 complement genes was conducted. The expression and methylation of nine complement genes in a murine MASH model were examined using quantitative RT-PCR and pyrosequencing.
Results
Methylome and transcriptome analyses of liver biopsies revealed significant (P<0.05) hypermethylation and downregulation of C1R, C1S, C3, C6, C4BPA, and SERPING1, as well as hypomethylation (P<0.0005) and upregulation (P<0.05) of C5AR1, C7, and CD59, in association with the histological severity of MASLD. Furthermore, DNA methylation and the relative expression of nine complement genes in a MASH diet mouse model aligned with human data.
Conclusions
Our research provides compelling evidence that epigenetic alterations in complement genes correlate with MASLD severity, offering valuable insights into the mechanisms driving MASLD progression, and suggests that inhibiting the function of certain complement proteins may be a promising strategy for managing MASLD.

Citations

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  • NSD2 exacerbates metabolic dysfunction-associated steatotic liver disease progression by suppressing TFEB-mediated autophagy-lysosomal pathway
    Yuan Qiao, Yijia Zhang, Cuiting Sun, Qi Jin, Peng Qu, Zecheng Li, Yang Qiu, Hua Meng, Dantao Peng, Liang Peng
    Metabolism.2026; 174: 156416.     CrossRef
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    Junhua Xie, Jun Lai, Yanzhe Zhang, Ye Liu, Zhixiang Yan
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    Guadalupe Hernández-Martínez, Andrés Hernández-Oliveras, Ángel Zarain-Herzberg, Juan Santiago-García, Kieran Campbell
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Review

Steatotic liver disease

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
Clin Mol Hepatol 2025;31(Suppl):S51-S75.
Published online June 27, 2024
DOI: https://doi.org/10.3350/cmh.2024.0246
In managing metabolic dysfunction-associated steatotic liver disease, which affects over 30% of the general population, effective noninvasive biomarkers for assessing disease severity, monitoring disease progression, predicting the development of liver-related complications, and assessing treatment response are crucial. The advantage of simple fibrosis scores lies in their widespread accessibility through routinely performed blood tests and extensive validation in different clinical settings. They have shown reasonable accuracy in diagnosing advanced fibrosis and good performance in excluding the majority of patients with a low risk of liver-related complications. Among patients with elevated serum fibrosis scores, a more specific fibrosis and imaging biomarker has proved useful to accurately identify patients at risk of liver-related complications. Among specific fibrosis blood biomarkers, enhanced liver fibrosis is the most widely utilized and has been approved in the United States as a prognostic biomarker. For imaging biomarkers, the availability of vibration-controlled transient elastography has been largely improved over the past years, enabling the use of liver stiffness measurement (LSM) for accurate assessment of significant and advanced fibrosis, and cirrhosis. Combining LSM with other routinely available blood tests enhances the ability to diagnose at-risk metabolic dysfunction-associated steatohepatitis and predict liver-related complications, some reaching an accuracy comparable to that of liver biopsy. Magnetic resonance imaging-based modalities provide the most accurate quantification of liver fibrosis, though the current utilization is limited to research settings. Expanding their future use in clinical practice depends on factors such as cost and facility availability.

Citations

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  • Correspondence to editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease”
    Hye Won Lee, Seung Up Kim
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  • Preface
    Seung Up Kim
    Clinical and Molecular Hepatology.2024; 30(Suppl): S3.     CrossRef
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Reply to Correspondence

Steatotic liver disease

Reply to correspondence on “Prognosis of biopsy-confirmed metabolic dysfunction-associated steatotic liver disease: A sub-analysis of the CLIONE study”
Eileen Laurel Yoon, Dae Won Jun
Clin Mol Hepatol 2024;30(4):1033-1034.
Published online May 20, 2024
DOI: https://doi.org/10.3350/cmh.2024.0360

Citations

Citations to this article as recorded by  Crossref logo
  • Prognostic value of non-invasive fibrosis assessment scores in predicting mortality among individuals with metabolic dysfunction-associated steatotic liver disease
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  • 4,160 View
  • 34 Download
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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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  • Associations between systemic inflammatory biomarkers and metabolic dysfunction associated steatotic liver disease: a cross-sectional study of NHANES 2017–2020
    Xin Qiu, Shuang Shen, Nizhen Jiang, Yifei Feng, Guodong Yang, Donghong Lu
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    Shekhar Swaroop, Sagnik Biswas, Shubham Mehta, Arnav Aggarwal, Umang Arora, Samagra Agarwal, Amitkumar Chavan, Baibaswata Nayak, Shalimar
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  • Shared genetic architecture between metabolic dysfunction-associated steatotic liver disease and cardiometabolic traits comorbidities: a genome-wide pleiotropic and multi-omics study
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    Xin Qiu, Shuang Shen, Nizhen Jiang, Yifei Feng, Guodong Yang, Donghong Lu
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    Jieun Choi, Ye Rin Choi, Min Kyo Jeong, Hyun Ho Song, Jeong Seok Yu, Seol Hui Song, Jeong Ha Park, Min Ju Kim, Hyunjoon Park, Young Lim Ham, Sang Hak Han, Dong Joon Kim, Do Yup Lee, Ki Tae Suk
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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”
    Eileen Laurel Yoon, Dae Won Jun
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Correspondence

Steatotic liver disease

Correspondence on Editorial regarding “Identification of signature gene set as highly accurate determination of MASLD progression”
Sungju Jung, Sumin Yoon, Jong Hoon Park, Yeon-Su Lee, Kyung Hyun Yoo
Clin Mol Hepatol 2024;30(2):287-290.
Published online February 23, 2024
DOI: https://doi.org/10.3350/cmh.2024.0136

Citations

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  • The effects of next generation probiotics on metabolic dysfunction-associated steatotic liver disease: a parallel, double-blind, randomized, placebo-controlled trial
    Sung-Min Won, Hyunchae Joung, In Gyu Park, Sang Hak Han, Young Lim Ham, Ji Sook Han, Yoojin Kwon, Dong Joon Kim, Ki Tae Suk
    Journal of Translational 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
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Editorial

Steatotic liver disease

The gene expression signature of metabolic dysfunction- associated steatotic liver disease from a multiomics perspective
Carlos Jose Pirola, Silvia Sookoian
Clin Mol Hepatol 2024;30(2):174-176.
Published online February 5, 2024
DOI: https://doi.org/10.3350/cmh.2024.0082

Citations

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  • Early portal hypertension in metabolic dysfunction-associated steatotic liver disease: a concise review
    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
  • The effects of next generation probiotics on metabolic dysfunction-associated steatotic liver disease: a parallel, double-blind, randomized, placebo-controlled trial
    Sung-Min Won, Hyunchae Joung, In Gyu Park, Sang Hak Han, Young Lim Ham, Ji Sook Han, Yoojin Kwon, Dong Joon Kim, Ki Tae Suk
    Journal of Translational Medicine.2025;[Epub]     CrossRef
  • Correspondence on Editorial regarding “Identification of signature gene set as highly accurate determination of MASLD progression”
    Sungju Jung, Sumin Yoon, Jong Hoon Park, Yeon-Su Lee, Kyung Hyun Yoo
    Clinical and Molecular Hepatology.2024; 30(2): 287.     CrossRef
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  • 92 Download
  • 3 Web of Science
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Original Article

Steatotic liver disease

Identification of signature gene set as highly accurate determination of metabolic dysfunction-associated steatotic liver disease progression
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-Su Lee, Kyung Hyun Yoo
Clin Mol Hepatol 2024;30(2):247-262.
Published online January 26, 2024
DOI: https://doi.org/10.3350/cmh.2023.0449
Background/Aims
Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by fat accumulation in the liver. MASLD encompasses both steatosis and MASH. Since MASH can lead to cirrhosis and liver cancer, steatosis and MASH must be distinguished during patient treatment. Here, we investigate the genomes, epigenomes, and transcriptomes of MASLD patients to identify signature gene set for more accurate tracking of MASLD progression.
Methods
Biopsy-tissue and blood samples from patients with 134 MASLD, comprising 60 steatosis and 74 MASH patients were performed omics analysis. SVM learning algorithm were used to calculate most predictive features. Linear regression was applied to find signature gene set that distinguish the stage of MASLD and to validate their application into independent cohort of MASLD.
Results
After performing WGS, WES, WGBS, and total RNA-seq on 134 biopsy samples from confirmed MASLD patients, we provided 1,955 MASLD-associated features, out of 3,176 somatic variant callings, 58 DMRs, and 1,393 DEGs that track MASLD progression. Then, we used a SVM learning algorithm to analyze the data and select the most predictive features. Using linear regression, we identified a signature gene set capable of differentiating the various stages of MASLD and verified it in different independent cohorts of MASLD and a liver cancer cohort.
Conclusions
We identified a signature gene set (i.e., CAPG, HYAL3, WIPI1, TREM2, SPP1, and RNASE6) with strong potential as a panel of diagnostic genes of MASLD-associated disease.

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Editorials

Steatotic liver disease

Adding to the confusion in more than just the name
Jacob George
Clin Mol Hepatol 2023;29(4):973-976.
Published online September 18, 2023
DOI: https://doi.org/10.3350/cmh.2023.0367

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Steatotic liver disease

From nonalcoholic steatohepatitis, metabolic dysfunction-associated fatty liver disease, to steatotic liver disease: Updates of nomenclature and impact on clinical trials
Ming-Lun Yeh, Ming-Lung Yu
Clin Mol Hepatol 2023;29(4):969-972.
Published online September 18, 2023
DOI: https://doi.org/10.3350/cmh.2023.0359

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CMH : Clinical and Molecular Hepatology
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