Clinical and Molecular Hepatology

"Alcohol"

Original Article

Glutamate excreted by LepR⁺ BM-MSCs mitigates alcohol-associated liver disease by promoting IL-1R2⁺ monocyte migration: Young-Ri Shim, Hee-Hoon Kim, Min Jeong Kim, Jun-Hee Lee, Kyurae Kim, Sung Eun Choi, Katherine Po Sin Chung, Eunmi Lee, Kwang Woo Lee, Jihyo Byun, Jaewoo Oh, Jae Min Han, Jun Ho Byun, Jong-Eun Park, Won Kim, Young-Sun Lee, Won-Il Jeong; Received April 5, 2026 Accepted June 16, 2026 Published online June 18, 2026; DOI: https://doi.org/10.3350/cmh.2026.0425 [Accepted]

Abstract
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Background/Aims
Bone marrow mesenchymal stromal cells (BM-MSCs) exert diverse functions, including supporting alcohol detoxification and providing a niche for monocyte development. However, their role in regulating monocytes during alcohol-related liver disease (ALD) remains unclear. This study investigates how BM-MSCs orchestrate the egress of anti-inflammatory monocytes from BM to the liver in ALD.
Methods
Wild-type, leptin receptor (LepR)⁺ BM-MSC-specific Slc7a11 knockout, and natural killer (NK) cell-specific Grm5 knockout mice were fed an ethanol diet for 8 weeks. Tissue analyses were performed using single-cell RNA sequencing (scRNA-seq), immunostaining, and flow cytometry. Blood and liver samples from ALD patients were examined.
Results
scRNA-seq revealed a distinct population of BM-derived Ly6C^low hepatic macrophages expressing interleukin-1 receptor 2 (IL-1R2), an IL-1β decoy receptor, in ethanol-fed mice. In the BM, alcohol exposure upregulated the gene expression of alcohol-metabolizing enzymes (Adh1, Aldh2), xCT (Slc7a11), and chemokines (Cxcl9, Cxcl10) in LepR⁺ BM-MSCs, promoting NK cell recruitment and interferon-γ (IFN-γ) production via metabotropic glutamate receptor 5 (mGluR5) activation. Subsequently, IFN-γ enhanced IL-1R2 expression and suppressed CX₃CR1 in neighboring Ly6C^low BM monocytes, facilitating their hepatic migration. LepR⁺ BM-MSC-specific xCT and NK cell-specific mGluR5 knockout mice exhibited exacerbated liver injury and elevated blood IL-1β levels, while recombinant IL-1R2 administration improved ameliorated ALD in wild-type mice. Consistently, increased IL-1R2 levels were observed in plasma, CD14⁺CD16⁺ blood monocytes, and liver tissues of ALD patients.
Conclusions
We identified a BM-liver axis in which glutamate released by BM-MSCs activates mGluR5 in BM NK cells, driving IL-1R2⁺ monocyte migration to the liver and attenuating ALD progression.

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Research Letters

Burden of cardiovascular complications in steatotic liver disease in the United States: Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed; Clin Mol Hepatol 2026;32(3):e326-e330.
Published online March 25, 2026; DOI: https://doi.org/10.3350/cmh.2026.0249

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Extrahepatic mortality associated with chronic liver disease with or without cirrhosis from 2014 to 2024: Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed; Clin Mol Hepatol 2026;32(2):e194-e198.
Published online February 25, 2026; DOI: https://doi.org/10.3350/cmh.2026.0225

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Review

Emerging therapeutic regimens as alternatives to glucocorticoids for severe alcohol-associated hepatitis: a comprehensive review: Rahul Kumar, Sakktivel Elangovan, Sumeet K. Asrani; Clin Mol Hepatol 2026;32(2):599-619.
Published online February 20, 2026; DOI: https://doi.org/10.3350/cmh.2025.1163

Abstract
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Severe alcohol-associated hepatitis (SAH) is the most aggressive form of alcohol-associated liver disease and is associated with very high short-term mortality. It is characterized by the acute onset of jaundice in the context of ongoing alcohol use, most commonly defined by a Maddrey’s discriminant function ≥32 or a model for end-stage liver disease score ≥20. Despite its increasing global burden and substantial healthcare costs, therapeutic options remain limited, and outcomes are poor. The severity of liver failure, systemic inflammation, infectious complications, and extrahepatic organ dysfunction determines the prognosis in SAH. The pathophysiology of SAH is multifactorial, involving direct hepatotoxicity from alcohol metabolites, oxidative stress, dysregulated immune activation, gut dysbiosis with increased intestinal permeability, impaired hepatic regeneration, and genetic susceptibility. These interrelated mechanisms culminate in an exaggerated inflammatory response driven by macrophage activation and cytokine release, resulting in hepatocellular injury and multi-organ failure. Glucocorticoids remain the guideline-recommended standard of care for selected patients; however, their benefit is limited to modest short-term survival gains, with high rates of non-response and infection. Numerous investigational therapies targeting inflammation, oxidative stress, liver regeneration, bile acid signalling, epigenetic regulation, and the gut-liver axis have been evaluated, with largely disappointing results. Emerging approaches, including interleukin-22 agonists and epigenetic modulators such as larsucosterol, show promise but require validation in well-designed trials. This review synthesizes current evidence on the definition, prognostic assessment, and pathophysiology of SAH, critically appraises existing and emerging therapies, and highlights the need for combination strategies, improved patient stratification, and personalized treatment approaches.

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Gut–Liver Axis Failure in Critical Alcohol‐Associated Liver Disease: From ICU Secondary Hits to Microbiome‐Targeted Therapy
Yuting Zhang, Yiyu Wang, Yong Yang, Hong Mei, Xinxin Liu, Yuanxiu He, Song Qin, Banghai Feng, Ranjitsinh V. Devkar
Mediators of Inflammation.2026;[Epub] CrossRef

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Letters to the Editor

Navigating discordant non-invasive fibrosis assessments in metabolic dysfunction-associated steatotic liver disease: Implications for generalizability, clinical decision-making, and resource allocation: Letter to the editor on “Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement”: Jiajing Zhao, Liping Liu; Clin Mol Hepatol 2026;32(3):e300-e302.
Published online February 20, 2026; DOI: https://doi.org/10.3350/cmh.2025.0157

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Critical considerations on the study of normal-weight metabolic dysfunction-associated steatotic liver disease across diverse populations: Letter to the Editor on “Normal-weight metabolic dysfunction-associated steatotic liver disease: Reclassification, characteristics, and adverse liver outcomes across diverse populations”: Qingshang Li, Xiaona Hu, Yuanwen Chen, Zhijun Bao; Clin Mol Hepatol 2026;32(3):e309-e311.
Published online February 5, 2026; DOI: https://doi.org/10.3350/cmh.2026.0067

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Editorial

Rethinking lean metabolic dysfunction-associated steatotic liver disease: Unrecognized risk in lean populations: Editorial on “Normal-weight metabolic dysfunction-associated steatotic liver disease: Reclassification, characteristics, and adverse liver outcomes across diverse populations”: Donghee Kim, Anoushka Shenoy, Aijaz Ahmed; Clin Mol Hepatol 2026;32(3):1441-1443.
Published online January 27, 2026; DOI: https://doi.org/10.3350/cmh.2026.0056

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Original Article

DNMT1 facilitates the progression of metabolic dysfunction-associated steatotic liver disease 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, Kyoung-Jin Oh, Won Kim, Mirang Kim, on behalf of the Innovative Target Exploration of NAFLD (ITEN) Consortium; Clin Mol Hepatol 2026;32(3):1201-1224.
Published online January 27, 2026; DOI: https://doi.org/10.3350/cmh.2025.1099

Abstract
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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, 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.

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Sus scrofa domesticus reveals the genetic evolution of adaptive traits during early divergence
Bohan Rong, Naiqi Niu, Wencheng Zong, Run Zhang, Xiaomei Ma, Na Zhang, Zhentong Shen, Yu Pang, Xu Lin, Di Liu, Yulong Yin, Longchao Zhang, Xiuqin Yang
The Innovation Life.2026; : 100222. CrossRef
Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks
Zijin Sun, Yongchao Liu, Kai Wang, Haojia Zhang, Rui Zhou, Wei Shao
International Journal of Molecular Sciences.2026; 27(12): 5526. CrossRef

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Letter to the Editor

Clinical implications of discordant FIB-4 and LSM in MASLD: Integrating evidence and optimizing pathways: Letter to the editor on “Histological severity and hepatic outcomes in patients with metabolic dysfunction-associated steatotic liver disease and discrepant FIB-4 and liver stiffness measurement”: Deliang Huang, Jun Chen; Clin Mol Hepatol 2026;32(3):e294-e296.
Published online January 20, 2026; DOI: https://doi.org/10.3350/cmh.2026.0027

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Reply to Correspondence

Reply to correspondence on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”: Seol Hee Park, Wonhyo Seo; Clin Mol Hepatol 2026;32(3):e432-e433.
Published online January 9, 2026; DOI: https://doi.org/10.3350/cmh.2025.1469

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Microbial Biomarkers for the Prevention and Diagnosis of Alcoholic Liver Disease
Goo Hyun Kwon, Hyunjoon Park, Hyeong Seop Kim, Ki Kwang Oh, Jung A Eom, Kyeong Jin Lee, Min Ju Kim, Minsoo Kim, Jeong Su Kim, Sang Hak Han, Young Lim Ham, Ki Tae Suk
Microorganisms.2026; 14(2): 449. CrossRef

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Correspondence

RAB25 as a liver-selective modulator of endoplasmic reticulum stress in alcohol-associated liver disease: Correspondence to editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”: Zi-Bin Zhan, Xue-Wen Liu, Ze-Hua Li, Fan-Hong Zeng, Kun-Hao Bai, Jun Weng; Clin Mol Hepatol 2026;32(3):e354-e357.
Published online January 6, 2026; DOI: https://doi.org/10.3350/cmh.2025.1422

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Original Article

Outcomes of oral antidiabetic drugs in metabolic dysfunction-associated steatotic liver disease: a nationwide target trial emulation study: Heejoon Jang, Yeonjin Kim, Yoo Kyoung Lim, Dong Hyeon Lee, Sae Kyung Joo, Bo Kyung Koo, Gi-Ae Kim, Woojoo Lee, Stefano Romeo, Won Kim, Innovative Target Exploration of NAFLD (ITEN) consortium; Clin Mol Hepatol 2026;32(2):737-750.
Published online January 6, 2026; DOI: https://doi.org/10.3350/cmh.2025.1006

Background/Aims
Patients with concurrent type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD) face elevated cardiovascular risks. However, optimal oral antidiabetic drug (OAD) selection for this population remains unclear.
Methods
Using the Korean National Health Information Database, we conducted a target trial emulation comparing cardiovascular outcomes among patients with T2DM and MASLD (defined by fatty liver index ≥30) who initiated sodium-glucose cotransporter 2 (SGLT2) inhibitors, thiazolidinediones, dipeptidyl peptidase-4 (DPP-4) inhibitors, or sulfonylureas with metformin. The primary outcome was major adverse cardiovascular events (MACE), including cardiovascular mortality, nonfatal myocardial infarction, and nonfatal stroke.
Results
Among 71,071 patients (331,726 person-years), SGLT2 inhibitor users experienced a significantly lower MACE risk compared to sulfonylurea users (adjusted subdistribution hazard ratio [aSHR], 0.44; 95% confidence interval [CI], 0.31–0.62). SGLT2 inhibitors also demonstrated a lower MACE risk compared to thiazolidinediones (aSHR, 0.61; 95% CI, 0.39–0.96) and DPP-4 inhibitors (aSHR, 0.59; 95% CI, 0.42–0.83). Cardiovascular mortality risk was notably reduced with SGLT2 inhibitors compared to sulfonylureas (aSHR, 0.13; 95% CI, 0.03–0.50), thiazolidinediones (aSHR, 0.19; 95% CI, 0.04–0.86), and DPP-4 inhibitors (aSHR, 0.22; 95% CI, 0.06–0.84). Mediation analysis revealed that MASLD regression accounted for 8.7% of the total cardiovascular benefit when comparing SGLT2 inhibitors to sulfonylureas.
Conclusions
In patients with concurrent T2DM and MASLD, SGLT2 inhibitors demonstrated better cardiovascular outcomes compared to other OADs. These findings suggest that SGLT2 inhibitors may be the preferred OAD choice for cardiovascular risk reduction in this high-risk population.

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Longitudinal changes in fatty liver index, genetic susceptibility, and incident atrial fibrillation
Siyang Liu, Houde He, Hualan Chen, Hualin Duan, Ying Sun, Dan Deng, Zihao Gui, Lan Liu, Ningjian Wang, Jie Shen, Heng Wan
Clinica Chimica Acta.2026; 589: 121028. CrossRef

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Correspondence

Correspondence to editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”: Xue-Wen Liu, Zi-Bin Zhan, Yu Gong, Ze-Hua Li, Kun-Hao Bai, Jun Weng; Clin Mol Hepatol 2026;32(3):e349-e353.
Published online December 23, 2025; DOI: https://doi.org/10.3350/cmh.2025.1397

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Original Article

Normal-weight metabolic dysfunction-associated steatotic liver disease: 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; Clin Mol Hepatol 2026;32(2):646-660.
Published online December 12, 2025; DOI: https://doi.org/10.3350/cmh.2025.0851

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 cardiometabolic risk factor (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 China (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 with 0 CMRF ranged from 9.0 to 26.7% among normal-weight NAFLD patients, representing the discrepancy between MASLD and NAFLD definitions. Compared with the overweight/obese MASLD, the normalweight MASLD had increased all-cause mortality (normal-weight vs. overweight/obese, 23.44 and 13.80 per 1,000 person-years; P<0.001) but not LREs (2.81 and 2.59 per 1,000 person-years; P=0.54) in the Hong Kong Clinical Data Analysis and Reporting System cohort.
Conclusions
Normal-weight individuals with NAFLD demonstrated a lower distribution of CMRFs, resulting in the incomplete agreement between historical NAFLD and MASLD.

Citations

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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
Beyond BMI: Reassessing the Prevalence of Obesity in Patients With MASLD Under the Lancet Commission Diagnostic Criteria
Ru‐Tao Lin, Ren‐Qiang Zeng, Xu‐Ting Shen, Qin‐Mei Sun, Xin Xin, Jia‐Mei Chen, Yi‐Yang Hu, Qin Feng
Diabetes, Obesity and Metabolism.2026; 28(8): 6699. CrossRef
Metabolic Dysfunction-Associated Steatotic Liver Disease and Incretin Receptor Agonists: A Metabolic Approach to Halting Liver Disease Progression
Ludovico Abenavoli, Anna Giulia Loricchio, Ivo Lopez, Domenico Morano, Abdulrahman Ismaiel, Dan Lucian Dumitrascu, Francesco Luzza
Medicina.2026; 62(5): 986. CrossRef
Estimated Body Fat Percentage and Triglyceride‐Glucose Index for Identifying MASLD in Lean Asian Adults: A Cross‐Sectional Analysis
Xiang‐Ran Kong, Ya‐Li Chen, Rui Li, Lu‐Xiang Shang, Sha Sha
The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
MASLD and its lean phenotype
Kateřina Janstová, Denisa Kyselová, Pavel Trunečka
Vnitřní lékařství.2026; 72(4): 232. CrossRef

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Editorials

Ethanol‑specific stress and RAB25/GCN1 signaling: Emerging perspectives in alcohol‑associated liver disease: Editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”: Miaomiao Wu, Qianying Cheng, Li Zuo, Hua Wang; Clin Mol Hepatol 2026;32(3):1394-1396.
Published online December 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.1360

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Mechanistic insights into a noncanonical RAB25-GCN1 axis in ALD: Editorial on “RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression”: Seol Hee Park, Wonhyo Seo; Clin Mol Hepatol 2026;32(3):1390-1393.
Published online December 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.1346

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Review

Novel biomarkers for alcohol-associated liver disease and their implications across clinical settings: Kaanthi Rama, Vinay Jahagirdar, Francisco Idalsoaga, Hanna Blaney, S. Fisher Rhoads, Luis Antonio Díaz, Marco Arrese, Juan Pablo Arab; Clin Mol Hepatol 2026;32(2):443-463.
Published online November 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0921

Abstract
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Alcohol-associated liver disease (ALD) is a leading cause of preventable cirrhosis, hepatocellular carcinoma (HCC), and liver-related mortality, yet current laboratory and imaging tools detect only late-stage disease. This narrative review synthesizes emerging evidence on novel biomarkers that capture the multidimensional pathophysiology of ALD and discusses their utility for routine clinical practice. Traditional serum-based liver fibrosis markers (e.g., cytokeratin-18 fragments, Pro-C3, the enhanced liver fibrosis test) improve non-invasive staging risk beyond aminotransferases, while elastography techniques, such as vibration-controlled transient elastography and magnetic resonance elastography, can also quantify liver stiffness with high precision. Among novel mechanistic biomarkers, genetic polymorphisms in PNPLA3, TM6SF2, MBOAT7, HSD17B13, and polygenic risk scores define lifetime risk, whereas sex-specific hormonal milieus also modify susceptibility and progression. Moreover, gut dysbiosis signatures, including reduced Faecalibacterium prausnitzii, Akkermansia muciniphila, and a lower Firmicutes/Bacteroidetes ratio, and their metabolites (short-chain fatty acids, and bile acids, trimethylamine N-oxide) correlate with liver inflammation and fibrosis. Endocrine imbalances of cortisol, testosterone, and thyroid hormones further stratify metabolic vulnerability. Ultimately, multi-omics platforms (i.e., transcriptomics, lipidomics, proteomics, metabolomics, and epigenomics) can reveal distinct molecular signatures that predict steatohepatitis, fibrogenesis, and early HCC. Integrating these biomarkers enables phase-specific enrichment strategies, earlier intervention windows, adaptive dose-finding, and mechanismbased endpoints in ALD trials. Remaining challenges include assay standardization, validation across diverse cohorts, and incorporation into regulatory frameworks. Future work could evaluate cost-effectiveness and feasibility in routine clinical practice. Widespread adoption promises earlier diagnosis, personalized risk reduction, and more efficient drug development for this globally prevalent disorder.

Citations

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Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation
Senping Xu, Zhaoshan Zhang, Zhongquan Zhou, Jiawei Guo
Biology.2026; 15(2): 148. CrossRef
Review Article on: AI-Driven Precision Medicine in Liver Disease: Microbiome and Nanotechnology Integration
Rahul Kumar, Amritesh Kumar, Aayush Kumar Tiwari, MD Nasiruddin Khan, Mohit Kumar, Moidul Islam Judder
Pan-African Journal of Health and Psychological Sciences.2026;[Epub] CrossRef
N-acetylcysteine for patients with alcohol use disorder, post-traumatic stress disorder, and their co-occurrence: a systematic review of placebo-controlled randomized trials
Mohamed Awad E. Ahmed, Mufreh Amin, Yomna Emad Abdalla, Amr Abdelghani, Nourhan Eid, Aya Samy, Omar Kassar, Khalid Radwan Alsaadany, Mohamed Ezzat M. Mansour
BMC Psychiatry.2026;[Epub] CrossRef

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Original Article

RAB25/GCN1 signaling promotes endoplasmic reticulum stress to mediate alcohol-associated liver disease progression: Xue-Wen Liu, Zi-Bin Zhan, Ze-Hua Li, Yue Zhang, Xue-Yan Qiao, Xin-Ming Li, Xiang-Jing Liang, Kun-Hao Bai, Xian-Feng Xia, Fan-Hon Zeng, Yi Gao, Jun Weng; Clin Mol Hepatol 2026;32(1):200-220.
Published online September 8, 2025; DOI: https://doi.org/10.3350/cmh.2025.0559

Background/Aims
Endoplasmic reticulum (ER) stress in hepatocytes plays a causative role in alcohol-associated liver disease (ALD). The incomplete inhibition of ER stress by targeting canonical ER stress sensor proteins suggests the existence of noncanonical ER stress pathways in ALD pathology. This study aimed to delineate the role of RAB25 in ALD and its regulatory mechanism in noncanonical ER stress pathways.
Methods
RAB25 activation was examined in liver samples from ALD patients and ethanol-fed mice. The interaction between RAB25 and GCN1 was confirmed through mass spectrometry and co-immunoprecipitation (Co-IP) assays in vitro. The role of RAB25/GCN1 in promoting noncanonical ER stress in ALD was assessed both in vitro and in vivo.
Results
RAB25 expression was upregulated and specifically accumulated on the ER in ALD. Mass spectrometry and Co-IP assays confirmed that RAB25 interacts with GCN1, thereby activating a noncanonical ER stress pathway that facilitates ALD progression. Further analysis revealed that RAB25 interaction with GCN1 inhibits K33-ubiquitination-mediated degradation of GCN1, promotes GCN2 phosphorylation, and subsequently activates ATF4-mediated ER stress. This activation modulates lipid metabolism, mitochondrial function, and inflammation, thereby facilitating ALD progression. Knockdown of RAB25 in hepatocytes inhibited ER stress activation and mitigated associated mitochondrial dysfunction, excessive lipid synthesis, and the exaggerated inflammatory response in an ALD model.
Conclusions
Our findings demonstrate a causal role for RAB25-GCN1 signaling in activating the ER stress pathway, which contributes to ALD progression. This pathway may provide a proof-of-concept target for treating ALD and associated metabolic disorders.

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Sesaminol Ameliorates Metabolic and Alcohol‐Related Liver Injury by Activating the PPARα/Slc27a5 Axis‐Driven Hepatic Fatty Acid β‐Oxidation
Liujie Zheng, Jun Zhou, Haojie Jin, Yu Long, Yifan Zheng, Kunying Ding, Ziyi Zheng, Fen Zhuge, Zhengwei Fu, Yinhua Ni
Molecular Nutrition & Food Research.2026;[Epub] CrossRef

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Correspondence

SAFE score in chronic liver diseases: A tool for risk enrichment and personalized surveillance: Correspondence to 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”: Tung-Hung Su, Jia-Horng Kao; Clin Mol Hepatol 2026;32(3):e396-e398.
Published online September 1, 2025; DOI: https://doi.org/10.3350/cmh.2025.0940

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Letter to the Editor

Sex‑specific trends and demographic vs. epidemiologic drivers of alcohol‑related cirrhosis in United States, 2021–2040: Letter to the editor on "Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States": Kui Wang, Yunqing Zeng; Clin Mol Hepatol 2026;32(2):e155-e157.
Published online August 25, 2025; DOI: https://doi.org/10.3350/cmh.2025.0790

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Evaluation methods of hepatic steatosis: From conventional techniques to emerging biomarkers
Kengo Moriyama
World Journal of Hepatology.2026;[Epub] CrossRef
Divergent trajectories of inflammatory bowel disease in East, South, South-East and Central Asia: A comprehensive GBD 2021 analysis
Kui Wang, Yunqing Zeng, Shanshan Zhang, Yanqing Li
Journal of Translational Autoimmunity.2025; 11: 100325. CrossRef

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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

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Impact of Documented Social Vulnerability on Clinical Outcomes in Metabolic Dysfunction‐Associated Steatotic Liver Disease
Pojsakorn Danpanichkul, Yanfang Pang, Maria Inggriani, Supapitch Sirimangklanurak, Matheus Souza, Ahmad Anouti, Andrew F. Ibrahim, Nikki Duong, Thomas G. Cotter, Thomas A. Kerr, Donghee Kim, Mazen Noureddin, Karn Wijarnpreecha
Liver International.2026;[Epub] CrossRef
Improved survival and reduced alcohol‐associated hepatitis risk with renin‐angiotensin‐aldosterone system inhibitors in alcohol‐associated liver disease
Pojsakorn Danpanichkul, Yanfang Pang, Donghee Kim, Andrew F. Ibrahim, Primrose Tothanarungroj, Omar Al Ta'ani, Narathorn Kulthamrongsri, Kwanjit Duangsonk, Robert J. Wong, Daniel Q. Huang, Karn Wijarnpreecha, Mazen Noureddin, Suthat Liangpunsakul
Alcohol, Clinical and Experimental Research.2026;[Epub] CrossRef
Extrahepatic mortality associated with chronic liver disease with or without cirrhosis from 2014 to 2024
Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed
Clinical and Molecular Hepatology.2026; 32(2): e194. CrossRef
The global epidemiology of alcohol-associated liver disease
Pojsakorn Danpanichkul, Francisco Idalsoaga, Frank Murray, Juan Pablo Arab, Luis Antonio Díaz
Hepatology Communications.2026;[Epub] CrossRef
Contemporary epidemiology of metabolic dysfunction-associated steatotic liver disease
Do Han Kim, Donghyun Ko, Aijaz Ahmed, Donghee Kim
Expert Review of Gastroenterology & Hepatology.2026; 20(6): 603. CrossRef

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Reply to Correspondence

Reply to correspondence 2 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”: Dibin Liu; Clin Mol Hepatol 2026;32(2):e264-e266.
Published online June 17, 2025; DOI: https://doi.org/10.3350/cmh.2025.0604

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Correspondence

Correspondence to letter to the editor on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”: Pojsakorn Danpanichkul, Luis Antonio Diaz, Juan Pablo Arab, Amit G. Singal, Ju Dong Yang; Clin Mol Hepatol 2026;32(2):e246-e248.
Published online June 17, 2025; DOI: https://doi.org/10.3350/cmh.2025.0594

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Reply to Correspondence

Reply to correspondence 1 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”: Sung-Eun Kim; Clin Mol Hepatol 2026;32(1):e125-e127.
Published online June 4, 2025; DOI: https://doi.org/10.3350/cmh.2025.0536

2,794 View
28 Download

Letter to the Editor

Letter to the editor on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”: Dibin Liu; Clin Mol Hepatol 2026;32(2):e153-e154.
Published online May 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0537

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Reply to correspondence 2 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
Dibin Liu
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Clinical and Molecular Hepatology.2026; 32(2): e246. CrossRef

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Research Letter

Hydrophilic and lipophilic statin and clinical outcomes in individuals with alcohol-associated liver disease: Pojsakorn Danpanichkul, Donghee Kim, Benjamin Nah, Karn Wijarnpreecha, Suthat Liangpunsakul; Clin Mol Hepatol 2025;31(3):e273-e276.
Published online May 27, 2025; DOI: https://doi.org/10.3350/cmh.2025.0474

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Association of documented social deprivation with cardiovascular and liver outcomes in alcohol-associated liver disease
Pojsakorn Danpanichkul, Yanfang Pang, Andrew F. Ibrahim, Supapitch Sirimangklanurak, Allan Bueso, Daniel M. Simadibrata, Shu-Yen Chan, Karn Wijarnpreecha, Mazen Noureddin, Donghee Kim, Suthat Liangpunsakul
Alcohol.2026; 132: 24. CrossRef
Impact of Documented Social Vulnerability on Clinical Outcomes in Metabolic Dysfunction‐Associated Steatotic Liver Disease
Pojsakorn Danpanichkul, Yanfang Pang, Maria Inggriani, Supapitch Sirimangklanurak, Matheus Souza, Ahmad Anouti, Andrew F. Ibrahim, Nikki Duong, Thomas G. Cotter, Thomas A. Kerr, Donghee Kim, Mazen Noureddin, Karn Wijarnpreecha
Liver International.2026;[Epub] CrossRef
Improved survival and reduced alcohol‐associated hepatitis risk with renin‐angiotensin‐aldosterone system inhibitors in alcohol‐associated liver disease
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Alcohol, Clinical and Experimental Research.2026;[Epub] CrossRef
Liver, Cardiovascular and Infectious Outcomes in Alcohol‐Associated Liver Disease With Cardiometabolic Risk Factors
Pojsakorn Danpanichkul, Kwanjit Duangsonk, Yanfang Pang, Krittameth Rakwong, Peerapun Jit‐are‐roon, Phuuwadith Wattanachayakul, Thitiphan Srikulmontri, Benjamin Nah, Vincent L. Chen, Donghee Kim, Christos S. Mantzoros, Mazen Noureddin, Karn Wijarnpreecha
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Effect of varenicline on major adverse liver outcomes in alcohol‐associated liver disease: An exploratory analysis
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Alcohol, Clinical and Experimental Research.2025; 49(11): 2451. CrossRef

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Editorial

Rising burden of alcohol-associated liver disease and cancers: Insights into sex disparities and policy implications: Editorial on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”: Sung-Eun Kim; Clin Mol Hepatol 2026;32(1):439-442.
Published online May 15, 2025; DOI: https://doi.org/10.3350/cmh.2025.0516

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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
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Clinical and Molecular Hepatology.2026; 32(1): e96. CrossRef
Reply to correspondence 1 on “Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States”
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Hidden Burden of Alcohol Use Disorder in MASLD and MetALD: Clinical and Nomenclatural Implications
Yuri Cho
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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

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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
Liver, Cardiovascular and Infectious Outcomes in Alcohol‐Associated Liver Disease With Cardiometabolic Risk Factors
Pojsakorn Danpanichkul, Kwanjit Duangsonk, Yanfang Pang, Krittameth Rakwong, Peerapun Jit‐are‐roon, Phuuwadith Wattanachayakul, Thitiphan Srikulmontri, Benjamin Nah, Vincent L. Chen, Donghee Kim, Christos S. Mantzoros, Mazen Noureddin, Karn Wijarnpreecha
Liver International.2026;[Epub] CrossRef
The global epidemiology of alcohol-associated liver disease
Pojsakorn Danpanichkul, Francisco Idalsoaga, Frank Murray, Juan Pablo Arab, Luis Antonio Díaz
Hepatology Communications.2026;[Epub] CrossRef
Contemporary epidemiology of metabolic dysfunction-associated steatotic liver disease
Do Han Kim, Donghyun Ko, Aijaz Ahmed, Donghee Kim
Expert Review of Gastroenterology & Hepatology.2026; 20(6): 603. 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
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Extrahepatic manifestation of metabolic dysfunction-associated steatotic liver disease
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Original Articles

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.

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Xianhua Mao, Mindie H. Nguyen
Clinical and Molecular Hepatology.2026; 32(2): e219. CrossRef
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Sex disparities in alcohol-associated liver disease and subtype differences in alcohol-attributable cancers in the United States: Pojsakorn Danpanichkul, Yanfang Pang, Tanuj Mahendru, Primrose Tothanarungroj, Luis Antonio Díaz, Juan Pablo Arab, Pimtawan Jatupornpakdee, Mark D. Muthiah, Kwanjit Duangsonk, Won-Mook Choi, Daniel Q. Huang, Donghee Kim, Mazen Noureddin, Karn Wijarnpreecha, Suthat Liangpunsakul, Amit G. Singal, Ju Dong Yang; Clin Mol Hepatol 2025;31(3):1058-1070.
Published online April 11, 2025; DOI: https://doi.org/10.3350/cmh.2025.0169

Background/Aims
Harmful alcohol use is a substantial contributor to liver diseases, liver cancer, and extrahepatic neoplasms. Patterns of alcohol consumption have shifted over recent decades. This study evaluates trends in alcohol-associated liver disease (ALD) and alcohol-attributable cancers in the United States (US) from 2000 to 2021.
Methods
Using the methodological framework of the Global Burden of Disease Study 2021, we analyzed trends in incidence, prevalence, and mortality from ALD and alcohol-attributable cancers in the US.
Results
In 2021, there were 28,340 new cases of ALD, 227,730 prevalent cases, and 21,860 deaths attributed to ALD in the US. From 2000 to 2021, ALD incidence, prevalence, and mortality increased by 43%, 36%, and 79%, respectively. The age-standardized incidence and death rate of ALD rose disproportionately among females compared to males. For alcohol-attributable cancers, primary liver cancer, colorectal cancer, and esophageal cancer accounted for the largest share of deaths in 2021. Age-standardized death rates increased significantly for primary liver cancer (annual percent change [APC] 2.21%, 95% confidence interval [CI] 1.70–2.73%) and other pharyngeal cancer (APC 1.35%, 95% CI 1.08–1.62%).
Conclusions
The burden of ALD is substantial and continues to rise in the US, with a particularly notable increase among females. Mortality from alcohol-attributable cancers is also increasing, mainly driven by primary liver cancer and pharyngeal cancer. However, system-wise, gastrointestinal cancer had the highest death attributable to alcohol. These findings highlight the urgent need for public health strategies to tackle ALD, primary liver cancer, and alcoholattributable extrahepatic malignancies.

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Research Letter

Lipidomic analysis of alcohol use disorder patients revealed the biomarkers for alcohol-related liver disease susceptibility: Dongyao Wang, Hongwei Zhang, Yuxiao Tang; Clin Mol Hepatol 2025;31(3):e259-e262.
Published online April 2, 2025; DOI: https://doi.org/10.3350/cmh.2025.0227

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Special Issue

Steatotic liver disease

KASL clinical practice guidelines for the management of metabolic dysfunction-associated steatotic liver disease 2025: Won Sohn, Young-Sun Lee, Soon Sun Kim, Jung Hee Kim, Young-Joo Jin, Gi-Ae Kim, Pil Soo Sung, Jeong-Ju Yoo, Young Chang, Eun Joo Lee, Hye Won Lee, Miyoung Choi, Su Jong Yu, Young Kul Jung, Byoung Kuk Jang, on behalf of The Korean Association for the Study of the Liver (KASL); Clin Mol Hepatol 2025;31(Suppl):S1-S31.
Published online February 19, 2025; DOI: https://doi.org/10.3350/cmh.2025.0045

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Correspondence

Alcohol-related liver disease

Correspondence to editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000-2021”: Pojsakorn Danpanichkul, Luis Antonio Diaz, Kanokphong Suparan, Karn Wijarnpreecha, Juan Pablo Arab; Clin Mol Hepatol 2025;31(2):e200-e202.
Published online February 17, 2025; DOI: https://doi.org/10.3350/cmh.2025.0166

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Editorial

Alcohol-related liver disease

Burden of alcohol use disorder, alcohol-related liver disease, and alcohol-related liver cancer: Editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021: Youxin Wang, Noriko Oza, Jazleen Leo, Ashok Choudhury, Daniel Q. Huang; Clin Mol Hepatol 2025;31(2):654-657.
Published online February 10, 2025; DOI: https://doi.org/10.3350/cmh.2025.0133

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Correspondence to editorial on “Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000-2021”
Pojsakorn Danpanichkul, Luis Antonio Diaz, Kanokphong Suparan, Karn Wijarnpreecha, Juan Pablo Arab
Clinical and Molecular Hepatology.2025; 31(2): e200. CrossRef

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Letters 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”: Chi-Kuei Hsu, Po-Yu Huang, Chih-Cheng Lai; Clin Mol Hepatol 2025;31(3):e247-e248.
Published online February 6, 2025; DOI: https://doi.org/10.3350/cmh.2025.0073

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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

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Original Articles

Alcohol-related liver disease

Global epidemiology of alcohol-related liver disease, liver cancer, and alcohol use disorder, 2000–2021: Pojsakorn Danpanichkul, Luis Antonio Díaz, Kanokphong Suparan, Primrose Tothanarungroj, Supapitch Sirimangklanurak, Thanida Auttapracha, Hanna L. Blaney, Banthoon Sukphutanan, Yanfang Pang, Siwanart Kongarin, Francisco Idalsoaga, Eduardo Fuentes-López, Lorenzo Leggio, Mazen Noureddin, Trenton M. White, Alexandre Louvet, Philippe Mathurin, Rohit Loomba, Patrick S. Kamath, Jürgen Rehm, Jeffrey V. Lazarus, Karn Wijarnpreecha, Juan Pablo Arab; Clin Mol Hepatol 2025;31(2):525-547.
Published online January 9, 2025; DOI: https://doi.org/10.3350/cmh.2024.0835

Background/Aims
Alcohol represents a leading burden of disease worldwide, including alcohol use disorder (AUD) and alcohol-related liver disease (ALD). We aim to assess the global burden of AUD, ALD, and alcohol-attributable primary liver cancer between 2000–2021.
Methods
We registered the global and regional trends of AUD, ALD, and alcohol-related liver cancer using data from the Global Burden of Disease 2021 Study, the largest and most up-to-date global epidemiology database. We estimated the annual percent change (APC) and its 95% confidence interval (CI) to assess changes in age-standardized rates over time.
Results
In 2021, there were 111.12 million cases of AUD, 3.02 million cases of ALD, and 132,030 cases of alcohol-attributable primary liver cancer. Between 2000 and 2021, there was a 14.66% increase in AUD, a 38.68% increase in ALD, and a 94.12% increase in alcohol-attributable primary liver cancer prevalence. While the age-standardized prevalence rate for liver cancer from alcohol increased (APC 0.59%; 95% confidence interval [CI] 0.52 to 0.67%) over these years, it decreased for ALD (APC –0.71%; 95% CI –0.75 to –0.67%) and AUD (APC –0.90%; 95% CI –0.94 to –0.86%). There was significant variation by region, socioeconomic development level, and sex. During the last years (2019–2021), the prevalence, incidence, and death of ALD increased to a greater extent in females.
Conclusions
Given the high burden of AUD, ALD, and alcohol-attributable primary liver cancer, urgent measures are needed to prevent them at both global and national levels.

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High Steatosis-Associated Fibrosis Estimator scores predict hepatocellular carcinoma in viral and non-viral hepatitis and metabolic dysfunction-associated steatotic liver disease: Tung-Hung Su, Sheng-Shun Yang, Mei-Hsuan Lee, Wei-Yu Kao, Shang-Chin Huang, Fen-Fang Chen, Francis SK Poon, Lung-Wen Tsai, Yi-Ting Chen, Che Lin, Weichung Wang, W Ray Kim, Jia-Horng Kao; Clin Mol Hepatol 2025;31(3):796-809.
Published online January 6, 2025; DOI: https://doi.org/10.3350/cmh.2024.0822

Background/Aims
There are no hepatocellular carcinoma (HCC) surveillance recommendations for non-viral chronic liver diseases (CLD), such as metabolic dysfunction-associated steatotic liver disease (MASLD). We explored the Steatosis-Associated Fibrosis Estimator (SAFE) score to predict HCC in MASLD and other CLD etiologies.
Methods
Patients with various CLDs were included from medical centers in Taiwan. The SAFE score, consisting of age, body mass index, diabetes, and laboratory data, was calculated at baseline, and patients were traced for new development of HCC. The predictability of the SAFE score for HCC was analyzed using the sub-distribution hazard model with adjustments for competing risks.
Results
Among 12,963 CLD patients with a median follow-up of 4 years, 258 developed HCC. The SAFE score classifies 1-, 3-, and 5-year HCC risk regardless of CLD etiologies. High (≥100) and intermediate (0–100) SAFE scores increased 11 and 2 folds HCC risks compared to low (<0) SAFE scores. Combining two lower risk tiers (SAFE<100), a high SAFE score (≥100) was associated with a 7.5-fold risk of HCC (adjusted sub-distributional hazard ratio [aSHR] 7.54; 95% confidence interval (CI) 5.38–10.60). A high SAFE score increased the risks of HCC in subgroups of viral hepatitis, non-viral hepatitis (aSHR 11.10; 95% CI 3.97–31.30) and MASLD (aSHR 4.23; 95% CI 1.43–12.50). A hospital cohort (n=8,103) and a community MASLD cohort (n=120,166) validated the high SAFE score (≥100) for HCC risk prediction.
Conclusions
The SAFE score stratifies high risks for HCC in CLD patients regardless of etiologies and helps to select at-risk candidates for HCC surveillance.

Citations

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Editorial

Steatotic liver disease

Vibration-controlled transient elastography in shaping the epidemiology and management of steatotic liver disease: Editorial on “Current burden of steatotic liver disease and fibrosis among adults in the United States, 2017–2023”: Xiao-Dong Zhou, Terry Cheuk-Fung Yip, Daniel Q Huang, Mark Dhinesh Muthiah, Mazen Noureddin, Ming-Hua Zheng; Clin Mol Hepatol 2025;31(2):620-624.
Published online December 26, 2024; DOI: https://doi.org/10.3350/cmh.2024.1131

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Alimentary Pharmacology & Therapeutics.2026; 63(1): 70. CrossRef
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Xiao‐Dong Zhou, Yusuf Yilmaz, Ming‐Hua Zheng
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Original Article

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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Reviews

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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Viral hepatitis

Mechanisms of hepatocellular carcinoma and cirrhosis development in concurrent steatotic liver disease and chronic hepatitis B: Saisai Zhang, Lung-Yi Mak, Man-Fung Yuen, Wai-Kay Seto; Clin Mol Hepatol 2025;31(Suppl):S182-S195.
Published online November 21, 2024; DOI: https://doi.org/10.3350/cmh.2024.0837

Abstract
PDF

Chronic hepatitis B (CHB) poses a major global public health challenge and is a leading cause of cirrhosis and liver cancer. Hepatic steatosis is common in individuals with CHB compared to the non-CHB population and is particularly prevalent in hepatitis B virus (HBV)-endemic regions, affecting about one-third of CHB patients. The interaction between hepatic steatosis and CHB-related disease progression is complex and still under debate. Evidence demonstrates that co-existing steatosis may worsen liver fibrosis while paradoxically increasing the likelihood of achieving better HBV control. In particular, despite the association of steatotic liver disease (SLD) with lower HBV viral loads and higher rates of HBsAg seroclearance, the coexistence of CHB and SLD can potentially accelerate liver disease progression. Factors such as fat deposition, lipotoxicity, oxidative stress, and chronic inflammation in SLD may foster a pro-fibrotic and pro-carcinogenic environment, accelerating the disease progression. Additionally, loss of global DNA methylation, changes in the immune microenvironment, and genetic susceptibility further contribute to the development of CHB-related cirrhosis and hepatocellular carcinoma (HCC). This review examines the mechanisms driving liver disease progression and the heightened risk of cirrhosis and HCC in patients with concurrent CHB and steatotic liver disease, underscoring the importance of prioritizing antiviral therapy for CHB in addition to addressing SLD.

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Alcohol-related liver disease

Alcohol-associated liver disease: Natural history, management and novel targeted therapies: Edilmar Alvarado-Tapias, Elisa Pose, Jordi Gratacós-Ginès, Ana Clemente-Sánchez, Hugo López-Pelayo, Ramón Bataller; Clin Mol Hepatol 2025;31(Suppl):S112-S133.
Published online October 31, 2024; DOI: https://doi.org/10.3350/cmh.2024.0709

Abstract
PDF

Alcohol consumption is a leading cause of preventable morbidity and mortality worldwide and the primary cause of advanced liver disease. Alcohol use disorder is a chronic, frequently relapsing condition characterized by persistent alcohol consumption despite its negative consequences. Alcohol-associated liver disease (ALD) encompasses a series of stages, from fatty liver (steatosis) to inflammation (steatohepatitis), fibrosis, and, ultimately, liver cirrhosis and its complications. The development of ALD is complex, involving both genetic and environmental factors, yet the exact mechanisms at play remain unclear. Alcohol-associated hepatitis (AH), a severe form of ALD, presents with sudden jaundice and liver failure. Currently, there are no approved targeted therapies able to interfere in the pathogenesis of ALD to stop the progression of the disease, making alcohol abstinence the most effective way to improve prognosis across all stages of ALD. For patients with advanced ALD who do not respond to medical therapy, liver transplantation is the only option that can improve prognosis. Recently, AH has become an early indication for liver transplantation in non-responders to medical treatment, showing promising results in carefully selected patients. This review provides an update on the epidemiology, natural history, pathogenesis, and current treatments for ALD. A deeper insight into novel targeted therapies investigated for AH focusing on new pathophysiologically-based agents is also discussed, including anti-inflammatory and antioxidative stress drugs, gut-liver axis modulators, and hepatocyte regenerative molecules.

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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

Citations

Citations to this article as recorded by

Advances in Diagnostic and Therapeutic Strategies for Metabolic Dysfunction-Associated Steatotic Liver Disease
Ryan Njeim, Omar Abureesh, Ali Sohail, Ryan Tam, Liliane Deeb
Livers.2026; 6(3): 35. CrossRef

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Crossref

Editorial

Alcohol-related liver disease

The urgent need for multidisciplinary approaches in managing alcohol-associated liver disease: Editorial on “The prognostic impact of psychiatric intervention on alcohol-associated liver disease: The UK Biobank cohort study”: Soon Sun Kim, Jae Youn Cheong; Clin Mol Hepatol 2025;31(1):316-318.
Published online October 7, 2024; DOI: https://doi.org/10.3350/cmh.2024.0847

7,050 View
68 Download

Correspondence

Steatotic liver disease

Correspondence to editorial on “Optimal cutoffs 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”: Jung Hwan Yu, Seung Up Kim; Clin Mol Hepatol 2025;31(1):e52-e54.
Published online September 24, 2024; DOI: https://doi.org/10.3350/cmh.2024.0815

9,317 View
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Letter to the Editor

Steatotic liver disease

Letter to the editor on “Bariatric intervention improves metabolic dysfunction-associated steatohepatitis in patients with obesity: A systematic review and meta-analysis”: Xiao-Song Li, Xi-Ping Shen, Hang Li; Clin Mol Hepatol 2025;31(1):e15-e16.
Published online September 12, 2024; DOI: https://doi.org/10.3350/cmh.2024.0784

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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
Clinical and Molecular Hepatology.2025; 31(1): e103. CrossRef

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Correspondence

Steatotic liver disease

Correspondence to editorial on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”: Hayeon Kim, Min Jeong Park, Myeong Gyu Kim, Kyungim Kim; Clin Mol Hepatol 2024;30(4):989-991.
Published online August 27, 2024; DOI: https://doi.org/10.3350/cmh.2024.0705

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Reply to correspondence on “Comparison of glucagon-like peptide-1 receptor agonists and thiazolidinediones on treating nonalcoholic fatty liver disease: a network meta-analysis”
Tian-Yi Ren, Mohammed Eslam, Jian-Gao Fan
Clinical and Molecular Hepatology.2024; 30(4): 1039. CrossRef

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Original Articles

Alcohol-related liver disease

The prognostic impact of psychiatric intervention on alcohol-associated liver disease: The UK Biobank cohort study: Keungmo Yang, Sunghwan Kim, Hyun Yang, Sheng-Min Wang, Bumseok Jeong, Hyun Kook Lim, Si Hyun Bae; Clin Mol Hepatol 2024;30(4):929-942.
Published online August 27, 2024; DOI: https://doi.org/10.3350/cmh.2024.0278

Background/Aims
Alcohol-associated liver disease (ALD) is a public health concern. ALD patients often have psychiatric comorbidities, but the effects of psychiatric interventions on ALD are not well-established. This study explores the prognostic impact of psychiatric intervention on ALD within UK Biobank cohort.
Methods
This population-based study included 2,417 ALD patients from the UK Biobank cohort. Psychiatric intervention was defined by a consultation with psychiatrists during hospitalization or a history of medication related to alcohol use disorder and psychiatric comorbidities. Survival analysis was conducted, incorporating propensity score matching (PSM), to precisely assess the impact of psychiatric intervention.
Results
Among 2,417 ALD patients, those with F10 (mental disorders due to alcohol) codes had poorer survival outcomes. Psychiatric intervention significantly improved the outcomes of both all-cause and liver-related mortality and reduced the incidence of liver cirrhosis. In subgroup or 2-year landmark analyses, psychiatric intervention consistently showed a survival benefit in ALD patients. In the multivariate analysis, psychiatric intervention was identified as a favorable prognostic factor (hazard ratio, 0.780; P=0.002 after PSM).
Conclusions
This study demonstrates the favorable effect of psychiatric intervention in ALD patients with psychiatric comorbidities. These findings emphasize the importance of integrated management for ALD patients to address both their medical and psychiatric aspects. Therefore, we suggest the potential benefits of early psychiatric interventions in improving survival outcomes in ALD.

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Trends in Concurrent Psychiatric Comorbidities in Alcohol-Associated Liver Disease: A Nationwide Study from 2015–2023
Shu-Yen Chan, Yee Hui Yeo, Hyunseok Kim, Molly Delk, Natchaya Polpichai, Pojsakorn Danpanichkul, Peng-Sheng Ting
Digestive Diseases and Sciences.2026; 71(4): 1493. CrossRef
Educational video modules for alcohol use disorder: A scalable tool to bridge the treatment gap in hepatology
Zi-Xiang Jin, Nian-Zhe Sun
World Journal of Hepatology.2026;[Epub] CrossRef
The urgent need for multidisciplinary approaches in managing alcohol-associated liver disease: Editorial on “The prognostic impact of psychiatric intervention on alcohol-associated liver disease: The UK Biobank cohort study”
Soon Sun Kim, Jae Youn Cheong
Clinical and Molecular Hepatology.2025; 31(1): 316. CrossRef

9,743 View
175 Download
3 Web of Science
Crossref

Steatotic liver disease

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, Young-Joo Jin, Jihyun An, Hee Yeon Kim, Miyoung Choi, Dae Won Jun, Mi Na Kim, Ji Won Han, Han Ah Lee, Jung Hwan Yu, Seung Up Kim; Clin Mol Hepatol 2024;30(Suppl):S117-S133.
Published online August 21, 2024; DOI: https://doi.org/10.3350/cmh.2024.0392

Background/aims
Opinions differ regarding vibration-controlled transient elastography and magnetic resonance elastography (VCTE/MRE) cut-offs for diagnosing advanced fibrosis (AF) in patients with non-alcoholic fatty liver disease (NAFLD). We investigated the diagnostic performance and optimal cut-off values of VCTE and MRE for diagnosing AF.
Methods
Literature databases, including Medline, EMBASE, Cochrane Library, and KoreaMed, were used to identify relevant studies published up to June 13, 2023. We selected studies evaluating VCTE and MRE regarding the degree of liver fibrosis using liver biopsy as the reference. The sensitivity, specificity, and area under receiver operating characteristics curves (AUCs) of the pooled data for VCTE and MRE for each fibrosis stage and optimal cut-offs for AF were investigated.
Results
A total of 19,199 patients from 63 studies using VCTE showed diagnostic AUC of 0.83 (95% confidence interval: 0.80–0.86), 0.83 (0.80–0.86), 0.87 (0.84–0.90), and 0.94 (0.91–0.96) for ≥F1, ≥F2, ≥F3, and F4 stages, respectively. Similarly, 1,484 patients from 14 studies using MRE showed diagnostic AUC of 0.89 (0.86–0.92), 0.92 (0.89–0.94), 0.89 (0.86–0.92), and 0.94 (0.91–0.96) for ≥F1, ≥F2, ≥F3, and F4 stages, respectively. The diagnostic AUC for AF using VCTE was highest at 0.90 with a cut-off of 7.1–7.9 kPa, and that of MRE was highest at 0.94 with a cut-off of 3.62–3.8 kPa.
Conclusions
VCTE (7.1–7.9 kPa) and MRE (3.62–3.8 kPa) with the suggested cut-offs showed favorable accuracy for diagnosing AF in patients with NAFLD. This result will serve as a basis for clinical guidelines for non-invasive tests and differential diagnosis of AF.

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