Background/Aims In adults with steatotic liver disease (SLD), the hepatic impact of transitioning between combustible cigarettes (CCs) and noncombustible nicotine or tobacco products (NNTPs) remains unclear. We examined CC-NNTP transitions and liver-related events (LREs).
Methods From the Korean National Health Insurance Service, 502,198 adults with SLD and at least one cardiometabolic risk factor completing health screenings during both 2012-2013 and 2019-2020 were followed through December 2023. Seven mutually exclusive groups were defined by CC status and NNTP use; the primary outcome was LRE, including hepatocellular carcinoma and liver cirrhosis. Cox proportional hazards regression, propensity-score matching (PSM), and counterfactual mediation analysis were performed.
Results Among 502,198 participants (mean age 57.9 years; 65.6% male), 2,549 LREs occurred over a median 3.0-year follow-up. Compared with never-smokers, continuous CC smokers without NNTP use had the highest LRE risk (aHR, 1.51; 95% confidence interval (CI), 1.34-1.70), followed by CC initiators (1.45; 1.17-1.79) and CC quitters (1.28; 1.12-1.46) without NNTPs. CC quitters with NNTP use showed a lower LRE risk than continuous CC smokers without NNTP use in the full cohort (aHR, 0.65; 95% CI, 0.43-0.99), but this association was not statistically significant under PSM (aHR, 0.65; 95% CI, 0.39-1.09). Within-group PSM of NNTP versus nonuse was nonsignificant across all CC categories.
Conclusions CC cessation was associated with lower LRE risk than continued CC smoking, even among those who transitioned to NNTPs. However, NNTP use showed no independent protective association, supporting complete tobacco/nicotine abstinence as the preferred goal.
Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) is the most common chronic liver disease worldwide, associated with considerable clinical and economic burden. Early detection and timely intervention of Metabolic Dysfunction Associated Steatohepatitis (MASH) remains a key cornerstone of management. Traditionally, histopathology assessment is central to the characterization of MASH disease activity and fibrosis, albeit with inherent limitations. The advent of artificial intelligence (AI) has provided transformative tools to augment many aspects of MASH diagnostics, including histology assessment. New technologies enabling digitalization of pathology slides and allowing for further AI assisted model analysis have helped to address some of the previous limitations. In this review, we highlight the key AI assisted digital pathology tools, including utility, performance and clinical impact. Limitations and real-world considerations in adopting these AI tools are also explored.
Yu Shi, Ruoqi Zhou, Seung Up Kim, Terry Cheuk-Fung Yip, Salvatore Petta, Elisabetta Bugianesi, Masato Yoneda, Manuel Romero-Gomez, Emmanuel Tsochatzis, Philip Newsome, Hannes Hagström, George Boon-Bee Goh, Wah-Kheong Chan, José-Luis Calleja, Jerome Boursier, Arun J. Sanyal, Jian-Gao Fan, Laurent Castera, Victor de Lédinghen, Michelle Lai, Xiao-Dong Zhou, Vincent Wai-Sun Wong, Ming-Hua Zheng, on behalf of VCTE-Prognosis Study Group
Clin Mol Hepatol 2026;32(3):1333-1348. Published online May 20, 2026
Background/Aims Liver stiffness measurement (LSM) is a key tool for risk stratification in metabolic dysfunction-associated steatotic liver disease (MASLD), yet static thresholds fail to capture dynamic transition across risk strata. We aimed to characterize LSM-risk transitions and develop a time-updated, individualized model for predicting state transitions, liver-related events and death (LREs/death).
Methods In a real-world MASLD cohort, we applied a multi-state, time-homogeneous Markov model to quantify annual transition probabilities and mean state occupancy times across LSM-defined low-, intermediate-, and high-risk strata. A Markov model incorporating age, sex, type 2 diabetes (T2D), hypertension was used to generate individualized, time-updated risk trajectories and probabilities of LREs/death.
Results Among 11,514 MASLD individuals with ≥2 vibration-controlled transient elastography assessments, the low-risk category demonstrated notable stability, with 92% remaining unchanged at 1 year and a mean occupancy time of 8.43 years (95% confidence interval [CI] 7.94–8.95). Contrarily, the intermediate-risk category was highly dynamic, with only 39% remaining unchanged after 1 year and a mean occupancy time of 0.92 years (95% CI 0.88–0.96). T2D, hypertension, and obesity substantially shorten low-risk occupancy time, whereas antidiabetic medication was associated with more favorable transitions. Finally, we developed a dynamic, multi-state Markov model integrating longitudinal LSM-defined risk states with relevant covariates to generate individualized predictions of state transitions and risks of LREs/death.
Conclusions LSM-based strata in MASLD represent distinct and meaningful dynamic trajectories. In particular, the marked instability of the intermediate-risk state supports more frequent reassessment. By quantifying transition pathways and time-updated risks of LREs/death, this model may inform the personalized surveillance intervals and risk-adapted management.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide and is closely linked to systemic metabolic disorders. In addition to their classical role in hemostasis, platelets are increasingly recognized as active regulators of inflammation and immune responses, yet their contribution to MASLD pathogenesis remains incompletely defined. This review synthesizes current knowledge on how metabolic disturbances and gut microbiota dysbiosis trigger platelet hyperactivation and intrahepatic recruitment. We examined the mechanisms by which activated platelets exacerbate steatosis, amplify inflammation through interactions with immune cells, promote fibrogenic remodeling through hepatic stellate cell activation, and contribute to hepatocarcinogenesis. In the context of MASLD-associated hepatocellular carcinoma, platelet involvement may occur through both inflammation/fibrogenic remodeling–mediated and direct tumor-regulatory mechanisms. Furthermore, the therapeutic potential of antiplatelet agents, particularly aspirin, in attenuating disease progression has been evaluated. We conclude that targeting platelet-related pathways may represent a promising therapeutic strategy to interrupt the interplay between metabolic dysfunction and liver injury in MASLD.
Hepatitis B virus (HBV) remains a major cause of chronic liver diseases, especially in the Asia-Pacific region. In recent decades, coinfection with hepatitis C virus (HCV) and coexistence with metabolic dysfunction-associated steatotic liver disease (MASLD) have emerged as significant clinical concerns among HBV-infected patients. Although global HBV vaccination programs and curative therapies for HCV have led to a marked decline in HBV/HCV coinfection, MASLD is rapidly becoming the predominant comorbidity due to the global surge in metabolic risk factors. HBV/HCV coinfection typically results in more severe liver damage, with unique challenges in antiviral treatment and risk of HBV reactivation post-HCV clearance. In contrast, HBV/MASLD overlap demonstrates complex metabolic-viral interactions that may influence viral replication, hepatitis B surface antigen seroclearance, fibrosis progression, and risk of hepatocellular carcinoma. This review critically compares the epidemiology, clinical outcomes, and management strategies of HBV patients with concurrent HCV or MASLD, while addressing current research gaps and proposing directions for future investigations.
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
Citations to this article as recorded by
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
Obesity and its related metabolic comorbidities, including type 2 diabetes, metabolic dysfunction-associated steatotic liver disease, and cardiovascular disease, are increasingly recognized as heterogeneous and multisystemic disorders. Despite the significant benefits in glycemic control and weight loss exhibited by GLP-1 receptor agonists (GLP-1RAs), their limitations have initiated the development of engineered multi-agonist therapies targeting additional nutrient-stimulated hormonal (NUSH) pathways. Dual and triple peptide-based co-agonists combining glucagon-like peptide-1 (GLP-1) with glucose-dependent insulinotropic polypeptide (GIP), glucagon, amylin, or peptide YY have demonstrated superior metabolic efficacy in preclinical and clinical studies. Tirzepatide (GLP-1/GIP dual agonist), CagriSema (GLP-1/amylin dual agonist), and retatrutide (GLP-1/GIP/glucagon triple agonist) have achieved unprecedented levels of weight loss and glycemic improvement, with certain agents also demonstrating hepatic, cardiovascular, and inflammatory benefits. Non-peptidyl oral GLP-1 RAs such as orforglipron, offer novel formulation strategies to enhance treatment accessibility and adherence. Multi-agonist incretin-based therapies represent a paradigm shift in the management of obesity and metabolic diseases. These agents offer broad clinical utility beyond glucose lowering by mimicking the pleiotropic hormonal responses observed after bariatric surgery. These therapies are poised to emerge as key components of precision metabolic medicine. This review article explores the mechanistic basis, pharmacological characteristics, and clinical data supporting the use of engineered NUSH-based peptide therapies for obesity and its related metabolic disorders, with particular emphasis on recent progress in the development and clinical application of dual and triple agonists.
Citations
Citations to this article as recorded by
Glucagon-like peptide-1 and dual/triple receptor agonists in the treatment of metabolic dysfunction-associated steatotic liver disease: advances in mechanistic research Xinyi Lu, Li Yang Frontiers in Medicine.2026;[Epub] CrossRef
Le Bich Hang Pham, Taeeung Kim, Seoyoung Kim, Yun Seok Kim, Jiyeon Kim, Kyeongseon Kim, Hyeonwoo Lim, Wan Seob Shim, Byoungmo Kim, So-Yeol Yoo, Jae-Young Lee, Murim Choi, Won Kim, Keon Wook Kang, Jeeyeon Lee
Clin Mol Hepatol 2026;32(1):318-338. Published online November 17, 2025
Background/Aims Ferroptosis, recently emerged as a new cell death modality characterized by iron-dependent peroxidation of lipids, has been explored in various diseases. However, detection of ferroptosis, particularly in chronic liver disease models, is hampered by the lack of universal ferroptosis markers and limited number of fluorescence sensors for in vivo ferroptosis.
Methods In this study, we developed TTM-4 as a highly sensitive near-infrared (NIR) fluorescent probe to detect ferroptosis.
Results TTM-4 exhibited turn-on fluorescence upon viscosity change, enabling visualization of lipid peroxidation (LPO) in ferroptotic hepatocytes and liver tissue samples with greater sensitivity than BODIPY 581/591 C11. Timelapse live-cell imaging of erastin-treated cells revealed real-time LPO dynamics involving cytosolic lipid droplets (cLDs), endoplasmic reticulum, and nuclear LDs in a chronological order. Further gene expression analysis of 216 liver tissue samples from the NCBI GEO database showed a significant increase in CIDEC concurrent with TTM-4 fluorescence during progression to metabolic dysfunction-associated steatotic hepatitis (MASH). TTM-4, with its low toxicity and turn-on NIR emission during ferroptosis, also enabled in vivo visualization of ferroptosis in liver injury and metabolic dysfunction-associated steatotic liver disease (MASLD) models.
Conclusions Our findings suggest that TTM-4 enables monitoring of ferroptosis in MASLD and would aid in early MASH diagnosis.
Citations
Citations to this article as recorded by
Targeting ferroptosis to halt MASLD and MASH Fudi Wang Trends in Endocrinology & Metabolism.2026;[Epub] CrossRef
Joseph Rabbat, Boyu Yang, Hye Won Lee, Huapeng Lin, Emmanuel Tsochatzis, Salvatore Petta, Elisabetta Bugianesi, Masato Yoneda, Ming-Hua Zheng, Hannes Hagström, Jérôme Boursier, José Luis Calleja, George Boon-Bee Goh, Wah-Kheong Chan, Rocio Gallego-Durán, Arun J. Sanyal, Victor de Lédinghen, Philip N Newsome, Jian-Gao Fan, Laurent Castéra, Michelle Lai, Céline Fournier-Poizat, Grace Lai-Hung Wong, Mirko Zoncape, Grazia Pennisi, Angelo Armandi, Atsushi Nakajima, Wen-Yue Liu, Ying Shang, Marc de Saint-Loup, Elba Llop, Kevin Kim Jun Teh, Carmen Lara-Romero, Amon Asgharpour, Sara Mahgoub, Mandy Sau-Wai Chan, Clemence M Canivet, Manuel Romero-Gomez, Vincent Wai-Sun Wong, Seung Up Kim, Terry Cheuk-Fung Yip
Clin Mol Hepatol 2026;32(1):289-304. Published online November 11, 2025
Background/Aims Current guidelines recommend a 2-step approach for identifying advanced fibrosis in metabolic dysfunction-associated steatotic liver disease (MASLD), using Fibrosis-4 index (FIB-4) followed by liver stiffness measurement (LSM) via vibration-controlled transient elastography (VCTE). However, some patients may exhibit discordant results. This study evaluates the histological severity and outcomes in patients with discordant FIB-4 and LSM results.
Methods This secondary analysis of the VCTE-Prognosis study included 12,950 patients evaluated for MASLD at 16 tertiary centers, of whom 2,915 underwent liver biopsy. Patients were categorized into four groups based on established FIB-4 (1.3) and LSM (8 kPa) cutoffs.
Results F3–F4 fibrosis was observed in 6.4%, 13.7%, 30.6%, and 62.4% in low-FIB-4-low-LSM (n=6,403), high-FIB-4-low-LSM (n=3,017), low-FIB-4-high-LSM (n=1,363), and high-FIB-4-high-LSM (n=2,167) groups, respectively. During a median follow-up of 47.4 months, 248 patients experienced hepatic decompensation, hepatocellular carcinoma, liver transplantation, or liver-related death. The incidence rates of liver-related events (LREs) were 0.67, 1.19, 2.58, and 21.30 per 1,000 person-years, respectively. Compared to low-FIB-4-low-LSM patients, those with low-FIB-4-high-LSM (adjusted subdistribution hazard ratio [aSHR] 4.12) and high-FIB-4-high-LSM (aSHR 21.38) had a significantly higher risk of LREs, while high-FIB-4-low-LSM patients did not. Similar findings were observed when hepatic decompensation and hepatocellular carcinoma were analyzed separately.
Conclusions Approximately 30% of patients in tertiary centers exhibit discordant FIB-4 and LSM results, with LSM more likely reflecting true severity. While some patients with discordant results may have advanced fibrosis, the overall incidence of LREs remains low.
Citations
Citations to this article as recorded by
Are FIB-4 and liver stiffness measurement interchangeable for HCC risk stratification in MASLD? Yimeng Zhou, Xue Meng JHEP Reports.2026; : 101852. CrossRef
High Prevalence of Metabolic Dysfunction–Associated Steatohepatitis With Significant Fibrosis in Primary Care and Endocrinology Clinics Srilaxmi Kalavalapalli, Eddison Godinez Leiva, Andrea Ortiz Rocha, Anu Sharma, Diana Barb, Nathaly Cuervo‐Pardo, Kelly Y. Chun, Toni R. Prezant, Margery A. Connelly, Jens T. Rosenberg, Joseph R. Grajo, Fernando Bril, Kenneth Cusi Diabetes, Obesity and Metabolism.2026; 28(7): 6184. CrossRef
The Evolution of MASLD Management: From Revised Nomenclature to Disease-Modifying Therapies Karolina Kornatowska, Szymon Kopciał, Mateusz Wiekiera, Adrianna Wiekiera, Paweł Budzik, Mateusz Tyniec, Kamal Morshed Gastroenterology Insights.2026; 17(2): 33. CrossRef
Background/Aims The first metabolic dysfunction-associated steatotic liver disease (MASLD) drug was approved with an unsatisfactorily small effect size. This study aimed to determine key factors impacting the cost-effectiveness of a new hypothetical MASLD drug as well as its treatment efficacy.
Methods A Markov model reflecting the natural history of MASLD was developed, incorporating fibrosis progression, cardiovascular disease risk, and mortality. Treatment effect of drug X (with $20,000 of annual cost) was assumed to achieve a ≥1 stage fibrosis regression, with a 25% gap of effect size in regression rate over non-treatment in the first year. The incremental cost-effectiveness ratio (ICER) over a 20-year horizon was estimated. And sensitivity analyses were conducted to explore uncertainty and identify influential factors.
Results In the base case analysis, drug X provided an incremental gain of 1.32 quality-adjusted life years (QALYs) and 1.20 life years compared to the non-treatment, with an ICER of $68,010/QALY–below the $100,000/QALY willingnessto- pay threshold, indicating that drug X treatment is cost-effective. Two-way sensitivity analysis further highlighted that the drug should achieve at least a 15% initial regression gap and maintain a minimum 3% sustained durability gap to remain cost-effective. In addition baseline fibrosis stage distribution also acted as an influencing factor.
Conclusions Long-term sustained durability of the hypothetical drug, patient distribution based on baseline fibrosis stage, as well as initial treatment response rate are key factors that influence the cost-effectiveness of new MASLD drugs.
Citations
Citations to this article as recorded by
The MASLD Journey in the General Population: Linkage‐to‐Care and Patient‐Reported Uptake of Fibrosis Risk Assessment Joo Hyun Oh, Jun‐Hyuk Lee, Sang Bong Ahn, Eunjoo Kwon, Eileen L. Yoon, Hyo Young Lee, Seon Cho, Dae Won Jun Liver International.2026;[Epub] CrossRef
Jiyi Choi, Moon Gyeong Yoon, Se Ha Jang, Geum Ok Baek, Hyun Sun Jung, Na-Rae Lee, Choong Hwan Lee, Ji Eun Han, Jae Youn Cheong, Jung Woo Eun, Soon Sun Kim
Clin Mol Hepatol 2026;32(1):239-257. Published online October 27, 2025
Background/Aims Gut microbiome plays a pivotal role in metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis, yet, associated functional mechanisms and host responses of specific microbial species remain insufficiently characterized. This study investigated the Bacteroides eggerthii therapeutic effects on MASLD by integrating multi-omics analysis and experimental validation in a Western diet (WD)-induced mouse model.
Methods Candidate strains were identified using 16S rRNA gene sequencing of fecal samples from individuals with and without MASLD or obesity. B. eggerthii, a species significantly depleted in both groups, was selected for functional evaluation. Male C57BL/6J mice were fed a WD or WD supplemented with B. eggerthii (WD+B) for 12 weeks. Liver histology, serum biochemistry, fecal microbiome and metabolome profiling, and hepatic and intestinal transcriptomic analyses were performed. Anti-steatotic effects of B. eggerthii–derived metabolites were validated in vitro.
Results Bacteroides eggerthii supplementation significantly improved liver weight, inflammation, fibrosis, and steatosis in WD+B group compared to WD alone. PICRUSt-based LEfSe analysis revealed choloylglycine hydrolase activity enrichment in gut microbiota, and strain-specific qPCR confirmed colonization in mouse colon. Integrated transcriptomic analyses revealed lipid and bile acid signaling pathway restoration, including CD36, FXR, and FGF15. Untargeted metabolomics identified elevated 2-hydroxyisocaproic acid (HICA) as a strain-derived metabolite in feces and B. eggerthii culture supernatants. In vitro, HICA significantly reduced lipid accumulation in free fatty acid-induced steatosis models.
Conclusions Bacteroides eggerthii ameliorates MASLD via gut-liver axis modulation, including bile acid metabolism and hepatic lipid signaling. These underscore its therapeutic potential and highlight HICA as a novel microbiome-derived metabolite with anti-steatotic activity.
Citations
Citations to this article as recorded by
Letter to the Editor: Circadian and microbial misalignment in metabolic dysfunction-associated steatotic liver disease - mechanistic insights and chronotherapeutic potential Christos Savvidis, Ioannis Ilias World Journal of Experimental Medicine.2026;[Epub] CrossRef
Decoding the Gut–Fat–Heart Axis: From Molecular Communication Networks to Clinical Translation Strategies Zijin Sun, Wei Shao, Haojia Zhang, Kai Wang, Yongchao Liu, Rui Zhou International Journal of Molecular Sciences.2026; 27(12): 5596. CrossRef
Metabolic dysfunction–associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease, has become the most common form of chronic liver disease in children. The spectrum of pediatric MASLD ranges from simple steatosis to steatohepatitis, fibrosis, cirrhosis, and in rare cases, hepatocellular carcinoma. Its pathogenesis involves a complex interplay among genetic, epigenetic, and environmental factors, along with alterations in the gut microbiota and its associated metabolites. Given the staggering prevalence and the distinct etiopathogenesis of pediatric MASLD, characterization of the gut microbiota and microbial products could facilitate the development of diagnostic tools and inform targeted therapeutic strategies. Current research on the gut microbiome in the context of pediatric MASLD is limited by small sample size, inadequate use of liver biopsy, methodological inconsistencies in sequencing, and confounding effects from metabolic comorbidities. In this review, we summarize clinical studies on alterations in the gut microbiota and microbial products (short-chain fatty acids, bile acids, and ethanol) that impact the pathogenesis of pediatric MASLD. We discuss the therapeutic potential of dietary modification, pharmacological treatments, and probiotics in improving disease progression by summarizing current clinical studies. Enhancing our understanding of the gut-liver axis may aid in the development of effective therapeutic strategies for pediatric MASLD.
Citations
Citations to this article as recorded by
Obesity, Metabolic Syndrome and MASLD in Children: Inflammation as the Missing Link—A Short Narrative Review Mihaela-Andreea Podeanu, Claudiu Marinel Ionele, Raluca Elena Sandu, Ion Rogoveanu, Mioara Desdemona Stepan, Carmen Elena Niculescu, Sergiu-Marian Cazacu, Ștefănița Bianca Vintilescu Life.2026; 16(2): 310. CrossRef
Artificial intelligence for metabolic dysfunction-associated steatotic liver disease diagnosis: A systematic review Ruijuan Wang, Chang Liu, Mei Xue, Jun Qian, Yue Hu Computers in Biology and Medicine.2026; 208: 111619. CrossRef
Effects of metabolic syndrome on pulmonary infection in pediatric bronchial asthma: a narrative review Li He, Yang Ye Frontiers in Pediatrics.2026;[Epub] CrossRef
Microbial metabolites at the nexus of gut-brain communication and neurodevelopmental disorders Yupeng Lai, Ming Zhang, Dandan Lang, Enfu Tao Frontiers in Nutrition.2026;[Epub] CrossRef
Targeting the Human Gut Microbiota—Between Conventional Therapy and Precision Genetic Engineering Naomi-Adina Ciurea, Laura Mahdi, Annarita Graziani, Agostino Di Ciaula, Piero Portincasa, Mohamad Khalil Nutrients.2026; 18(12): 1958. CrossRef
Background/Aims Excessive lipid accumulation in hepatocytes is a critical cause of metabolic dysfunction-associated steatotic liver disease (MASLD) progression. Ankyrin repeat and SOCS box protein 3 (ASB3) is an E3 ubiquitin ligase that mediates diverse disease processes; however, the direct substrates of ASB3 in lipid metabolism and its role in MASLD remain unexplored.
Methods We generated ASB3 knockout mice fed a high-fat diet to induce MASLD. Oxygen consumption and fatty acid oxidation (FAO) were used to assess lipid metabolism. LC-MS/MS and IP were used to verify the ASB3 target protein. Correlation analysis was conducted on the cohort of MASLD patients vs. the control group.
Results Loss of the ASB3 E3 ubiquitin ligase in hepatocytes strengthens mitochondrial FAO, thereby influencing energy consumption to decrease triglyceride storage and lipid accumulation. Quantitative lysine ubiquitination proteomics revealed that ASB3 directly mediated the ubiquitin levels at two sites (K180 and K639) in carnitine palmitoyl transferase 1A (CPT1A), a rate-limiting enzyme of FAO, to induce CPT1A degradation. Moreover, both constitutive and hepatocyte-specific ASB3 knockout enhance FAO and delay lipid accumulation, liver steatosis, and MASLD progression in a CPT1A-dependent manner. Hepatic ASB3 deficiency also delays fibrosis in MASLD. Analysis of public databases and liver tissue samples from MASLD patients revealed that ASB3 was highly expressed in MASLD patients and was negatively correlated with CPT1A.
Conclusions Our study reveals the key roles of ASB3 in the development of MASLD and suggests a novel therapeutic potential for MASLD.
Citations
Citations to this article as recorded by
Targeting the ASB3-CPT1A axis—a new player in combating metabolic dysfunction-associated steatotic liver disease: Editorial on “Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver diseas Yueying Yang, Ying Yang, Yan Lu Clinical and Molecular Hepatology.2026; 32(2): 957. CrossRef
The first genome-wide association study on pediatric obesity in Taiwan Hsin-Ru Wu, Ting-Yuan Liu, Chuan-Mu Chen, Fuu-Jen Tsai Journal of the Formosan Medical Association.2026;[Epub] CrossRef
Correspondence to editorial on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study” Xianhua Mao, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(2): e219. CrossRef
Correspondence to letter to the editor on “Molecular classification of hepatocellular carcinoma based on zoned metabolic feature and oncogenic signaling pathway” Tomoko Aoki, Naoshi Nishida, Masatoshi Kudo Clinical and Molecular Hepatology.2026; 32(2): e241. CrossRef
Mendelian randomization (MR), a powerful statistical tool for causal inference, has been widely applied in various fields of medical research, even extending to economics and psychology. In hepatology, MR has been utilized to identify risk factors and potential therapeutic targets for liver diseases, including metabolic dysfunction-associated steatotic liver disease, cholestatic and autoimmune liver diseases, and hepatobiliary cancer. MR can provide evidence of causation via associations between genetic variants, modifiable exposures and liver disease occurrence or outcomes, using large existing datasets. However, results from MR studies are sometimes scattered, biologically not plausible or even controversial between analyses, potentially reflecting a trend of inappropriate application of this method (e.g., inappropriate selection of genetic instruments, insufficient assessment of horizontal pleiotropy, compromised statistical power, and neglected genetic diversity among different populations), and thus hinder the translation of MR findings from bench to bedside. Assessing these critical issues and pinpointing bona fide evidence are essential but quite challenging for clinicians. In this review, we aim to introduce the MR method to hepatologists and provide a comprehensive overview of the current MR findings that are relevant for hepatologists. Furthermore, we will discuss how to evaluate the quality of MR publications, interpret MR findings, and illustrate good practice of using MR studies in hepatology.
Citations
Citations to this article as recorded by
Childhood Obesity and Age‐Related Diseases: A Systematic Review and Meta‐Analysis of Mendelian Randomization Evidence Haoxue Zhu, Xinghao Yi, Mengyu He, Siyi Wu, Ming Li, Shan Gao Pediatric Obesity.2026;[Epub] CrossRef
Association of genetically instrumented HMGCR inhibition with the therapeutic role of prostate cancer: a Mendelian randomization study and supporting in vitro experiments Xiaojie Hao, Jingjun Mu Frontiers in Pharmacology.2026;[Epub] CrossRef
Aspirin and hepatocellular carcinoma risk in metabolic dysfunction-associated steatotic liver disease: nationwide cohort study with genetic risk analysis Juhee Ahn, Moon Haeng Hur, Hyunjae Shin, Min Kyung Park, Sungho Won, Jeayeon Park, Yunmi Ko, Youngsu Park, Yun Bin Lee, Eun Ju Cho, Jeong-Hoon Lee, Su Jong Yu, Jung-Hwan Yoon, Yoon Jun Kim Clinical and Molecular Hepatology.2026; 32(1): 339. CrossRef
Integrative Mendelian randomization and experimental validation unveil novel druggable targets in primary biliary cholangitis Yinling Li, Huanhuan Xie, Zhenjie Zhuang, Xin Fang, Wenjun Yang, Yan Luo, Jiangyi Hu, Wei Wang, Haitao Wang, Xiaobing Dou, Junping Shi, Jin Yang European Journal of Pharmacology.2026; 1020: 178775. CrossRef
Integrated Plasma Proteomics and Functional Analyses Reveal Hepatic CDHR2 as a Potential Therapeutic Target in MASLD Yuanping Shi, Qi Huang, Yingning Liu, Xinlei Zhang, Feng Liu, Huiying Rao, Xueyao Han, Linong Ji, Xiantong Zou Diabetes, Obesity and Metabolism.2026; 28(5): 4303. CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Liver Aging Index: A Noninvasive Score for Liver Biological Aging and Liver‐Related Outcomes in Multicohorts Zhiyu Wu, Shanshan Wu, Shuyao Song, Yating Huang, Canqing Yu, Dianjianyi Sun, Pei Pei, Ling Yang, Yiping Chen, Huaidong Du, Robin Walters, Iona Millwood, Hao Xu, Xiaoming Yang, Junshi Chen, Seung Up Kim, Salvatore Petta, Atsushi Nakajima, Emmanuel Tsochat Aging Cell.2026;[Epub] CrossRef
Helicobacter pylori, peptic ulcer disease, and colorectal cancer: a prospective study with genome-wide interaction analysis and Mendelian randomization Ziqi Wan, Jiarui Mi, Xiaoyin Bai, Dong Wu, Sunny Hei Wong Infectious Agents and Cancer.2025;[Epub] CrossRef
Evaluating causal protective effect of dual GLP-1R/GIPR agonists on MASLD: A Mendelian randomization and colocalization study Yangke Cai, Siyuan Xie, Liyi Xu, Jiamin Chen, Jianting Cai European Journal of Pharmacology.2025; 1005: 178088. CrossRef
Integrative genome-wide analysis unveils the genetic landscape of gallstone disease and highlights novel loci with therapeutic potential Haotian Chen, Zhengye Liu, Hanze Du, Mixue Zheng, Ziqi Wan, Nan Zhao, Guanqiao Li, Xiaoyin Bai, Dong Wu, Jiarui Mi BMJ Open Gastroenterology.2025; 12(1): e001976. CrossRef
Correspondence to letter to the editor on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Hye Won Lee, Seung Up Kim Clinical and Molecular Hepatology.2026; 32(2): e244. CrossRef
Advancing metabolic risk profiling in chronic hepatitis B: Reply to correspondence on “Metabolic health in antiviral era of chronic hepatitis B” Shang-Chin Huang, Jia-Horng Kao Clinical and Molecular Hepatology.2026; 32(1): e117. CrossRef
Reply to correspondence on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues” Heejoon Jang, Won Kim Clinical and Molecular Hepatology.2026; 32(2): e254. CrossRef
Correspondence to editorial 2 on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues” Rui Huang, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(1): e85. CrossRef
Correspondence to editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Hye Won Lee, Seung Up Kim Clinical and Molecular Hepatology.2026; 32(1): e87. CrossRef
Background/Aims Information about the association of glucagon-like peptide-1 receptor (GLP-1RA) with liver and non-liver complications is insufficient in patients with type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD). We conducted a target trial emulation study to evaluate whether GLP-1RA decreases the risk of liver and non-liver outcomes.
Methods Patients with T2D and MASLD initiating GLP-1RA or dipeptidyl peptidase-4 inhibitor (DPP-4i) were included from 2013 to 2022 in Merative™ Marketscan® Research Databases. Primary outcomes included incidences of (1) hepatocellular carcinoma (HCC) and cirrhosis, and (2) cardiovascular disease (CVD), chronic kidney disease (CKD), and non-liver cancer. Inverse probability of treatment weighting was applied to balance baseline characteristics and Cox regression models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).
Results In the intention-to-treat design, GLP-1RA, compared with DPP-4i, had a significantly lower incidence (per 1,000 person-years) of HCC (0.8 vs. 1.7; HR 0.53, 95% CI 0.39–0.71), of cirrhosis (29.3 vs. 32.9; HR 0.91, 95% CI 0.86–0.96), of CVD (57.2 vs. 73.9; HR 0.90, 95% CI 0.86–0.95), of CKD (4.5 vs. 6.8; HR 0.73, 95% CI 0.64–0.84), and of non-liver cancer (16.9 vs. 22.9; HR 0.82, 95% CI 0.77–0.89). In the per-protocol design, significant inverse associations for these study outcomes still were observed, with HR 0.60–0.77.
Conclusions In this emulated target trial of nationwide patients with T2D and MASLD, GLP-1RA use, when compared with DPP-4i, was associated with a significantly lower risk of liver and non-liver complications.
Citations
Citations to this article as recorded by
Tirzepatide versus SGLT2 inhibitors for MASLD: a multi-institutional propensity score-matched cohort study Jheng-Yan Wu, Yu-Min Lin, Wan-Hsuan Hsu, Ting-Hui Liu, Ya-Wen Tsai, Po-Yu Huang, Min-Hsiang Chuang, Tsung Yu, Chih-Cheng Lai Hepatology International.2026; 20(2): 292. CrossRef
Impact of newer antihyperglycemic agents on hepatic complications: A systematic review and meta-analysis of data from 5.3 million patients with type 2 diabetes mellitus Jiwon Yang, Yeongseok Hwang, Jin-Sung Ju, Seungbong Han, Jihyun An, Ju Hyun Shim Hepatology.2026;[Epub] CrossRef
Association of Semaglutide Treatment With Liver Cirrhosis and Hepatocellular Carcinoma in Type 2 Diabetes: A Population‐Based Cohort Study Assaf Issachar, Talish Razi, Ilya Borochov, Hadar Duskin Bitan, Ronen Arbel Diabetes, Obesity and Metabolism.2026; 28(7): 5704. CrossRef
Early cancer risk reduction after GLP-1RA use: Signal or bias?: Letter to the editor on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic l Shio-Shin Jean, Chih-Cheng Lai Clinical and Molecular Hepatology.2026; 32(2): e163. CrossRef
Letter to the editor on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study” Chunyan Wang, Xu Han, Yinyan Li Clinical and Molecular Hepatology.2026; 32(2): e167. CrossRef
Correspondence to letter to the editor 1 on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study Xianhua Mao, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(2): e231. CrossRef
Correspondence to letter to the editor 2 on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study Xianhua Mao, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(2): e249. CrossRef
Letter to the editor on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study” Xingyu Yao Clinical and Molecular Hepatology.2026; 32(2): e165. CrossRef
Correspondence to editorial on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study” Xianhua Mao, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(2): e219. CrossRef
Reply to correspondence on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study” Xingyu Yao Clinical and Molecular Hepatology.2026; 32(2): e267. CrossRef
GLP-1RA may open a new era for MASLD treatment: Editorial on “Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target tria Ye Feng, Chengfu Xu Clinical and Molecular Hepatology.2026; 32(2): 924. CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Secular Trend in Glycaemic Management in Type 2 Diabetes Patients With and Without Cirrhosis Between 2000 and 2023: A Territory‐Wide Cohort Study Mary Yue Wang, Sherlot Juan Song, Nana Peng, Grace Lai‐Hung Wong, Vincent Wai‐Sun Wong, Jimmy Che‐To Lai, Terry Cheuk‐Fung Yip Alimentary Pharmacology & Therapeutics.2026;[Epub] CrossRef
GLP-1 receptor agonist–SGLT-2 inhibitor combination and risk of major adverse liver and cardiovascular outcomes in adults with MASLD and type 2 diabetes Xianhua Mao, Hong Fan, Man-Fung Yuen, Ramsey Cheung, Wai-Kay Seto, Mindie H. Nguyen Hepatology.2026;[Epub] CrossRef
Tumor microenvironment and metabolic reprogramming in MASLD-related hepatocellular carcinoma Vanilla X. Zhang, Tiffany C.-Y. Yu, Yu M. Tsui, Irene O.-L. Ng Trends in Molecular Medicine.2026;[Epub] CrossRef
Hepatic Events Prevention by Antihyperglycemic Therapies and Intervention Comparisons in Type 2 Diabetes: The HEPATIC-T2DM Network Meta-analysis Pedro Robson Costa Passos, Rodrigo Motta, Valbert Oliveira Costa Filho, Mariana Macambira Noronha, Roberto Cavalcante Venâncio, Guilherme Grossi Lopes Cançado, Amanda Adler, Jeremy F. Cobbold, Jeremy W. Tomlinson Diabetes Care.2026; 49(6): 1144. CrossRef
Predictors of Discordance Between Controlled Attenuation Parameter and Magnetic Resonance-Proton Density Fat Fraction in Hepatic Steatosis Dong Yun Kim, Hyung-Jin Rhee, Beom Kyung Kim Clinical and Translational Gastroenterology.2026;[Epub] CrossRef
Glucagon-Like Peptide-1 Receptor Agonist Use and Liver-Related Outcomes in Metabolic Dysfunction-Associated Steatotic Liver Disease and Type 2 Diabetes in the All of Us Research Program Erik Almazan, Jonggi Choi, Tushar Kamath, Vy H. Nguyen, Eric Przybyszewski, Jiunn Song, Allison Carroll, Megan Michta, Tracey G. Simon, Raymond T. Chung American Journal of Gastroenterology.2026;[Epub] CrossRef
Association between hemoglobin glycation index and new-onset diabetes mellitus in individuals with chronic liver disease: Findings from a prospective cohort study using CHARLS data Yanyan Mao, Hui Kong, Li Wang, Fangyan Liao, Xiangwen Li Medicine.2026; 105(27): e49567. CrossRef
Glucagon-like peptide-1 receptor agonists versus dipeptidyl peptidase-4 inhibitors after liver resection for hepatocellular carcinoma in patients with type 2 diabetes: a target trial emulation study Yan-Jun Xiang, Zong-Han Liu, Jin-Kai Feng, Ying-Yi Qin, Hong-Ming Yu, Yu-Qiang Cheng, Gang Chen, Jia-Yi Wu, Yong-Yi Zeng, Yu-Fu Tang, Jian-Hua Rao, Feng-Min Zhang, Shi-Ye Yang, Gui-Ran Wang, Lin-Sen Ye, Ren Lang, Jian-Hua Lin, Yi-Tao Zheng, Ye-Fan Mao, Ho Gut.2026; : gutjnl-2026-338462. CrossRef
Evaluating causal protective effect of dual GLP-1R/GIPR agonists on MASLD: A Mendelian randomization and colocalization study Yangke Cai, Siyuan Xie, Liyi Xu, Jiamin Chen, Jianting Cai European Journal of Pharmacology.2025; 1005: 178088. CrossRef
Impaired Thyroid Hormone Sensitivity is Associated with Increased
Risk of Liver Fibrosis in Euthyroid Population: A Cross-Sectional Analysis of
NHANES Xingyu Yao, Kaiwen Xiao, Hein Ko Oo Hormone and Metabolic Research.2025; 57(09): 511. CrossRef
Background/Aims Berberine ursodeoxycholate (HTD1801) has been shown to significantly reduce liver fat content (LFC) in an 18-week, placebo-controlled Phase 2 study in patients with metabolic dysfunction-associated steatohepatitis (MASH) and type 2 diabetes mellitus. The purpose of this assessment was to establish proof of concept in liver histologic improvement with HTD1801 treatment based on preclinical and clinical evidence.
Methods The efficacy of HTD1801 was evaluated in a preclinical MASH/dyslipidemia model (golden hamsters fed a high fat diet, eight/group) after six weeks of daily treatment. Additionally, in a secondary analysis of a Phase 2 clinical study, 100 patients with presumed MASH were evaluated by multiple noninvasive markers associated with MASH resolution and/or fibrosis improvement. These include magnetic resonance imaging proton density fat fraction (MRIPDFF; ≥30% LFC reduction), iron-corrected T1 (≥80 ms reduction), alanine aminotransferase (≥17 U/L reduction), weight loss (≥5% reduction), Fibrosis-4 index (shift to <1.3), and MASH resolution index (achieving ≥–0.67).
Results Preclinical findings in the MASH/dyslipidemia hamster model showed that HTD1801 significantly improved histologic fibrosis and the Nonalcoholic Fatty Liver Disease Activity Score to such a degree that improvements approximated the appearance of the normal controls. In the clinical study, 52% of HTD1801-treated patients achieved MRI response criteria compared to 24% of placebo (p<0.05). Dose-dependent improvements were observed across biomarkers, with more HTD1801-treated patients achieving response criteria associated with improvements in the histologic features of MASH.
Conclusions These findings suggest that HTD1801 has strong potential to produce histological improvements in patients with MASH.
Citations
Citations to this article as recorded by
Activation of Sirtuin 3, a Promising “Head Goose Molecule,” Triggers the Negentropic Mechanism for Treating Metabolic Diseases Hu Li, Tong Wang, Biao Dong, Zonggen Peng, Jiandong Jiang Engineering.2026; 60: 294. CrossRef
Standard-Dose Ursodeoxycholic Acid Improves Biochemical Liver Function and Fibrosis in Chronic Liver Disease: Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial Young Chang, Yong Kyun Cho, Young Seok Kim, Sung-Eun Kim, Gab Jin Cheon, Ji Hoon Kim, Hyun Yang, Won Kim, Sang Bong Ahn, Eileen L. Yoon, Jae Youn Cheong, Jin-Woo Lee, Moon Young Kim, Hyung Joon Kim, Sae Hwan Lee, Eun Young Cho, Na Ryung Choi, Hye Won Lee, Journal of Korean Medical Science.2026;[Epub] CrossRef
An overview on phytotherapeutics for metabolic syndrome: A journey from traditional knowledge to modern clinical validation Dolly Rani, Sandip Chatterjee, Pawan Kumar Goswami Journal of Diabetes & Metabolic Disorders.2026;[Epub] CrossRef
Mapping the global research output of Traditional Chinese Medicine in the treatment of metabolic dysfunction-associated steatotic liver disease: a comprehensive bibliometric analysis based on multiple databases (2000–2025) Da Wang, Mengwei Li, Rongting Zhao, Hui Wang, Hang Chen, Minshan Huang, Yingxue Shen, Lanqing Ma Frontiers in Medicine.2026;[Epub] CrossRef
Comparative efficacy of phase 2–3 therapies for non-cirrhotic metabolic dysfunction-associated steatohepatitis: An updated network meta-analysis Tsubasa Tsutsumi, Nicole Shu Ying Tang, Cheng Han Ng, Hiroyuki Suzuki, Nicholas L. Syn, N. Apoorva Sasikumar, Glenn Jun Kit Ho, Damien Chua, Jing Kai Tioh, Thanawin Pramotedham, Selvakumar Vigneshwaran, Peter Jin Sun Low, Joon Ho Moon, Dan Yock Young, Vin Med.2026; 7(5): 101077. CrossRef
Regulation of bile acids homeostasis: a feasible and versatile way to treat or diagnose liver disorders Qian-Qian Wu, Le-Ying Gao, Hui-Yi Feng, Hao-Lin Liu, Hui Gao, Wei Peng, Nan Li Frontiers in Nutrition.2026;[Epub] CrossRef
“Surrogates without substance?” Questioning the evidence for histologic improvement with HTD1801: Letter to the editor on “HTD1801 demonstrates promising potential for histologic improvements in metabolic dysfunction-associated steatohepatitis in both a p Zhihao Lei Clinical and Molecular Hepatology.2026; 32(2): e158. CrossRef
Letter to the editor on “HTD1801 demonstrates promising potential for histologic improvements in metabolic dysfunction-associated steatohepatitis in both a preclinical and phase 2 study” Xi-Lin Gao Clinical and Molecular Hepatology.2026; 32(2): e161. CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Molecular mechanisms and clinical applications of gut microbiota-derived bioactive compounds in metabolic dysfunction-associated fatty liver disease Chengyun Ma, Jing Wang, Xuanli Song, Xue Wang, Shuai Zong Frontiers in Immunology.2025;[Epub] CrossRef
Advancing metabolic risk profiling in chronic hepatitis B: Reply to correspondence on “Metabolic health in antiviral era of chronic hepatitis B” Shang-Chin Huang, Jia-Horng Kao Clinical and Molecular Hepatology.2026; 32(1): e117. CrossRef
Correspondence to editorial 1 on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues” Rui Huang, Mindie H. Nguyen Clinical and Molecular Hepatology.2026; 32(1): e83. CrossRef
Steatosis paradox: Unraveling pathways of suppressive effect of hepatic steatosis on hepatitis B virus Shang-Chin Huang, Jia-Horng Kao Biomedical Journal.2026; 49(3): 100969. CrossRef
The Chronic Hepatitis B and Metabolic Dysfunction-Associated Steatotic Liver Disease Paradox: Friend or Foe? Shang-Chin Huang, Tai-Chung Tseng Gut and Liver.2026; 20(3): 350. CrossRef
Insulin Resistance and Hepatocellular Carcinoma Development in Chronic Hepatitis B Patients Under Antiviral Therapy Dong Hyun Sinn, Kyung-Ah Kim, Jung Il Lee, Geum-Youn Gwak Journal of Korean Medical Science.2026;[Epub] CrossRef
Background/Aims Recently, the Korean Association for the Study of the Liver (KASL) introduced a noninvasive test-based approach that uses the fibrosis-4 (FIB-4) index followed by vibration-controlled transient elastography (VCTE) to identify high-risk patients with metabolic-associated steatotic liver disease (MASLD). In this study, the KASL two-step approach was validated by assessing the risk of liver-related event (LRE) development.
Methods We retrospectively analyzed 8,131 patients with MASLD who underwent VCTE between 2012 and 2020. The index date was defined as the date of the VCTE measurement. Using the KASL two-step approach (FIB-4 index and subsequent VCTE), patients were stratified into four groups (low-, intermediate-low-, intermediate-high-, and high-risk groups). Outcomes, including LREs such as decompensation (DCC) or hepatocellular carcinoma (HCC) were evaluated.
Results During the follow-up (median 46.6 months), 86 (1.1%) patients developed LREs (39 [0.5%] with DCC and 47 [0.6%] with HCC). The KASL two-step approach classified 67.6%, 17.7%, 5.7% and 9.0% of patients in the low-, intermediate-low-, intermediate-high-, and high-risk groups, respectively. The cumulative incidences of LREs increased proportionally according to risk stratification (0.07%, 0.10%, 0.29%, and 1.51% at 3 years and 0.35%, 0.26%, 1.94% and 5.46% at 5 years). The overall accuracy in predicting LREs ranged from 67.7–99.8%. The FIB-4 index and subsequent Agile3+, Agile 4, or FibroScan aspartate aminotransferase scores showed similar predictive abilities compared to the KASL approach.
Conclusions The KASL two-step approach is an effective and practical method for risk stratification in patients with MASLD, optimizing patient care through early identification of high-risk individuals.
Citations
Citations to this article as recorded by
Correspondence to editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Hye Won Lee, Seung Up Kim Clinical and Molecular Hepatology.2026; 32(1): e87. CrossRef
Risk stratification of metabolic dysfunction-associated steatotic liver disease: The KASL pathway: Editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” May Xuan Goh, Xin En Goh, Jarell Jie-Rae Tan, Vincent L Chen, Yu Jun Wong Clinical and Molecular Hepatology.2026; 32(1): 429. CrossRef
Risk Stratification of Chronic Kidney Disease in Adults Using Noninvasive Fibrosis Tests Based on the American Diabetes Association Algorithm Chan‐Young Jung, Hye Won Lee, Jung Il Lee, Han Ah Lee, Seung Up Kim Diabetes, Obesity and Metabolism.2026; 28(6): 5240. CrossRef
Letter to the editor on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Chunyan Wang, Jun Sun, Yinyan Li Clinical and Molecular Hepatology.2026; 32(2): e146. CrossRef
Correspondence to letter to the editor on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Hye Won Lee, Seung Up Kim Clinical and Molecular Hepatology.2026; 32(2): e244. CrossRef
The MASLD Journey in the General Population: Linkage‐to‐Care and Patient‐Reported Uptake of Fibrosis Risk Assessment Joo Hyun Oh, Jun‐Hyuk Lee, Sang Bong Ahn, Eunjoo Kwon, Eileen L. Yoon, Hyo Young Lee, Seon Cho, Dae Won Jun Liver International.2026;[Epub] CrossRef
Rethinking first-line screening in MASLD beyond the limitations of Fibrosis-4 index: Editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Han Ah Lee, Young Youn Cho, Hyung Joon Kim Clinical and Molecular Hepatology.2026; 32(2): 921. CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Predictors of Discordance Between Controlled Attenuation Parameter and Magnetic Resonance-Proton Density Fat Fraction in Hepatic Steatosis Dong Yun Kim, Hyung-Jin Rhee, Beom Kyung Kim Clinical and Translational Gastroenterology.2026;[Epub] CrossRef
Validation of combo ichroma as a reliable concentration-based alternative for AST and ALT measurement in liver disease monitoring Minsoo Kim, Su A Kim, Jeong Min Kim, Hee Young Kim, Ho Yeong Yoon, Sung Won Park, Daegyun Park, Ji Sook Han, Ki Tae Suk Methods.2025; 243: 66. CrossRef
Metabolic dysfunction-associated steatotic liver disease, formerly referred to as non-alcoholic fatty liver disease, is the most common liver disease in Western countries and has emerged as the leading indication for liver transplantation. Metabolic dysfunction-associated steatohepatitis (MASH), a more advanced stage, carries a high risk of progression to liver fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. Until recently, lifestyle intervention remained the mainstay of MASH management, with no pharmacological treatments specifically approved. However, advances in understanding its pathophysiological mechanisms have fueled numerous clinical trials, culminating in the Food and Drug Administration’s (FDA) approval of resmetirom as the first treatment for MASH in 2024. Additionally, many investigational drugs are nearing FDA approval or progressing through late-stage clinical trials. This review examines the current therapeutic landscape, highlights strategies for identifying patients suitable for liver-directed therapies in real-world settings, and discusses the challenges that remain.
Citations
Citations to this article as recorded by
Quzhou-sourced Fructus Aurantii ameliorates MASLD by modulating glycolysis-dependent M1 polarization in hepatic macrophages Junbin Yan, Yunmeng Nie, Menglu Ding, Mi Zhou, Tingyuan Li, Sumei Xu, Shuo Zhang Phytomedicine.2026; 150: 157572. CrossRef
Stimuli-responsive nanomedicines for hepatic diseases: mechanism, design, recent advances, and clinical translation Leyi Wang, Xue Zhang, Yinggang Li, Min Zhao, Gang Xu, Zhenyu Duan, Qiyong Gong, Kui Luo Journal of Controlled Release.2026; 390: 114522. CrossRef
Editorial: Combination Therapies for MASH: A Step Forward or More Complexity? Xiao‐Dong Zhou, Yusuf Yilmaz, Mazen Noureddin, Hung N. Luu, Ming‐Hua Zheng Alimentary Pharmacology & Therapeutics.2026; 63(6): 903. CrossRef
Combination therapies for metabolic dysfunction-associated steatohepatitis: challenges and opportunities Xiao-Dong Zhou, Qiong-Yue Fan, Christopher D Byrne, Giovanni Targher, Mark D Muthiah, Daniel Q Huang, Qin-Fen Chen, Mazen Noureddin, Wenhao Li, Vlad Ratziu, Rohit Loomba, Sven M Francque, Arun J Sanyal, Ming-Hua Zheng Gut.2026; 75(4): 815. CrossRef
Convergent Metabolic Pathways in MASH Therapeutics: An AMPK‐Centric Analysis Seungchan Choi, Jin‐Seok Jung, Yie‐sung Seo, Sungmin Song, Jeehye Ham, Hannah Chung, Yousef Ramadan, Kangchan Choi Journal of Cellular and Molecular Medicine.2026;[Epub] CrossRef
Clinical Utility of a 50% and 30% Decline in Magnetic Resonance Imaging-Proton Density Fat Fraction in Predicting Fibrosis Improvement in Metabolic Dysfunction-associated Steatohepatitis Rohit Loomba, Peter Chen-Yang Nikhil Daniel, Youxin Wang, Ricki Bettencourt, Egbert Madamba, Harris Siddiqi, Lisa Richards, Mildred D. Gottwald, Shibao Feng, Maya Margalit, Daniel Q. Huang Clinical Gastroenterology and Hepatology.2026;[Epub] CrossRef
The role and possible mechanism of intestinal fungi in the progression of chronic liver diseases Yirui Hu, Ye Yang, Shuyan Wang, Huikuan Chu npj Biofilms and Microbiomes.2026;[Epub] CrossRef
Artificial Intelligence, Real Results: AI Successfully Risk-Stratifies Patients with MASLD Cristian R. Perez, Mohamed A. Elfeki Digestive Diseases and Sciences.2026;[Epub] CrossRef
p53: from understanding its structure to advances in therapeutic targeting Wenhua Wang, Xia Liu, Hengqi Liu, Hassan Abolhassani, Han Yan, Huilai Zhang, Xianhuo Wang Signal Transduction and Targeted Therapy.2026;[Epub] CrossRef
Dyslipidemia in liver cirrhosis: Pathophysiology and emerging therapeutic approaches Jenyfer M Fuentes-Mendoza, Marcio J Concepción-Zavaleta, Jeny J Mendoza-Godoy, Luis A Concepción-Urteaga, Carlos O Martínez-Gutiérrez, José Paz-Ibarra World Journal of Hepatology.2026;[Epub] CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease Koral S. E. Richard, Sumati Rohilla, Reethika Gade, Fabio Arias, Oren Rom Current Atherosclerosis Reports.2026;[Epub] CrossRef
Metabolism-modulating nanoparticles for remodeling adipose-liver crosstalk to reverse liver fibrosis Ling-Feng Zhang, Su-Qing Liang, Qing-Wen Huang, Jia-Wen Ru, Ze-Quan Ding, Chun-Yu Zhang, Yi Wang, Tian-Jiao Zhou, Lei Xing, Xian Wu Cheng, Yu-Kyoung Oh, Hu-Lin Jiang Journal of Controlled Release.2026; 395: 115026. CrossRef
The Evolution of MASLD Management: From Revised Nomenclature to Disease-Modifying Therapies Karolina Kornatowska, Szymon Kopciał, Mateusz Wiekiera, Adrianna Wiekiera, Paweł Budzik, Mateusz Tyniec, Kamal Morshed Gastroenterology Insights.2026; 17(2): 33. CrossRef
Health inequity and the risk of MAFLD/MASLD Ziyan Pan, Abdulla Al Hassani, Khalid M. AlNaamani, Yasser Fouad, Munira Y. Altarrah, Mohammed Eslam Clinical Nutrition ESPEN.2026; 74: 103355. CrossRef
Predictors of Discordance Between Controlled Attenuation Parameter and Magnetic Resonance-Proton Density Fat Fraction in Hepatic Steatosis Dong Yun Kim, Hyung-Jin Rhee, Beom Kyung Kim Clinical and Translational Gastroenterology.2026;[Epub] CrossRef
Insights into Metabolic-Inflammatory Dual-targeting Effects of Huangqi Guizhi Wuwu Decoction on Diabetic Hepatopathy via Regulation of the AMPK-FASN/PI3K-AKT Axis Sheng-Wen Lu, Qi-Qi Zhao, Zhi-Bo Wang, Si-Fan Guo, Ying Cai, Xian Wang, Dan-Dan Xie, Zhen-Cai Hu, Shi-Wei Wang, Ai-Hua Zhang, Yu Guan, Shi Qiu World Journal of Traditional Chinese Medicine.2026;[Epub] CrossRef
The economic burden of MASH: comparison of healthcare resource utilization and costs in patients with probable MASH, without MASH, and with diagnosed MASH Caichen Zhong, Nana Boame, Semiu O. Gbadamosi, Maximilian Jara, Rakesh Luthra, Alex Salamun, Yu Hong, Abdalla Aly, Fernando Bril, Mary E. Rinella Expert Review of Pharmacoeconomics & Outcomes Research.2026;[Epub] CrossRef
Steatotic Liver Disease in Older Adults: Clinical Implications and Unmet Needs Daniel Clayton-Chubb, William W. Kemp, Ammar Majeed, Peter W. Lange, Jessica A. Fitzpatrick, Karl Vaz, John S. Lubel, Alexander D. Hodge, Joanne Ryan, John J. McNeil, Alice J. Owen, Robyn L. Woods, Stuart K. Roberts Nutrients.2025; 17(13): 2189. CrossRef
Tirzepatide in metabolic dysfunction-associated steatotic liver disease and steatohepatitis: a novel star on the horizon? Amedeo Lonardo, Ralf Weiskirchen Exploration of Drug Science.2025;[Epub] CrossRef
Timosaponin AIII from Anemarrhena asphodeloides binds and inhibits S100A8-mediated neutrophil infiltration and NET formation ameliorates MASH Yunfan Bai, Jingxin Ju, Ruishi Xie, Jing Li, Xinyi Zhao, Xiaoxue Fang, Ming Zhu, Xintian Lan, Haoming Luo International Immunopharmacology.2025; 166: 115539. CrossRef
Full Active Nanoplatform Restores ROS Homeostasis for Synergistic Therapy of Fatty Liver Disease via Dual Endogenous–Exogenous Pathways Ziyi Lin, Peng Xu, Yuehai Xu, Yixin Zheng, Huimin Li, Zixin Chen, Zhe Wang, Shaochen Song, Yuhao Liu, Zhao Yang, Ju Cui, Heyun Shen ACS Applied Materials & Interfaces.2025;[Epub] CrossRef
From mechanisms to management: Early detection and improved treatment of MASLD and its related hepatocellular carcinoma Dingwu Li, Xiang Zhang Hepatology Communications.2025;[Epub] CrossRef
Background/Aims Given the increase in prevalence of metabolic diseases, we investigated their long-term impacts on the outcomes of chronic hepatitis B (CHB) patients receiving nucleos(t)ide analogue (NA) treatment.
Methods We analyzed data from CHB patients for whom initiated NA treatment from 30 centers. We balanced patient characteristics with and without metabolic disease (diabetes, obesity, dyslipidemia, and hypertension) via propensity-score matching (PSM) to evaluate adverse outcomes.
Results The study included 4,500 patients. PSM yielded 909 pairs of patients with balanced characteristics. When stratified by the number of metabolic diseases, only patients with ≥2 metabolic diseases had an increased cumulative incidence of cirrhosis and overall death. However, when stratified by the presence of diabetes (regardless of the presence or number of other metabolic diseases), patients with diabetes (versus those without) had a significantly higher cumulative incidence of all outcomes: cirrhosis (P=0.009), hepatocellular carcinoma (HCC, P=0.023), and overall, liver-related, and non-liver-related death (P<0.001, P=0.026 and P<0.001, respectively). Having ≥2 metabolic diseases was associated with cirrhosis, overall death, and non-liver-related death but not HCC or liver-related death, while diabetes was significantly associated with a higher risk of all outcomes: cirrhosis (hazard ratio [HR]=3.75, P=0.004), HCC (HR=2.02, P=0.020), and overall, liver-related, and non-liver-related death (HR=2.53, P<0.001; HR=2.65, P=0.016; HR=2.38, P<0.001).
Conclusions Having two or more metabolic diseases was associated with a higher risk of cirrhosis, overall death, and non-liver-related death, but having diabetes as a single metabolic disease was significantly associated with all adverse outcomes including cirrhosis, HCC, and overall, liver-related, and non-liver-related death.
Citations
Citations to this article as recorded by
Type 2 diabetes mellitus as an independent predictor of significant fibrosis in treatment-naïve chronic hepatitis B patients with concurrent hepatic steatosis Jie Li, Liang Xu, Fajuan Rui, Sally Tran, Pei-Chien Tsai, Youwen Tan, Hidenori Toyoda, Qing-Lei Zeng, Huy Trinh, Yao-Chun Hsu, Tsunamasa Watanabe, Hiroshi Abe, Hiroyuki Motoyama, Yoko Yoshimaru, Takanori Suzuki, Taeang Arai, Masanori Atsukawa, Phillip Vut Hepatology.2026; 83(5): 1273. CrossRef
Advancing metabolic risk profiling in chronic hepatitis B: Reply to correspondence on “Metabolic health in antiviral era of chronic hepatitis B” Shang-Chin Huang, Jia-Horng Kao Clinical and Molecular Hepatology.2026; 32(1): e117. CrossRef
Metabolic health in antiviral era of chronic hepatitis B: Editorial on “Impacts of metabolic syndrome diseases on long-term outcomes of chronic hepatitis B patients treated with nucleos(t)ide analogues” Shang-Chin Huang, Jia-Horng Kao Clinical and Molecular Hepatology.2026; 32(1): 423. CrossRef
Diagnosis and management of metabolic dysfunction-associated steatohepatitis in patients with chronic hepatitis B infection Talal K Bhatti, Joseph K Lim World Journal of Gastroenterology.2026;[Epub] CrossRef
Diabetes Impairs the Virological Response in Patients with Chronic Hepatitis B: Glycemic Control as a Key Modifiable Risk Factor Aoyi Li, Yan Han, Guanglin Xiao, Zhiling Deng, Chaojing Wen, Ke Qiu, Taiyu He, Hong Ren Journal of Clinical Medicine.2026; 15(5): 1826. CrossRef
Antiviral Therapy Reduces Hepatocellular Carcinoma and Cirrhosis Risk in Chinese Chronic Hepatitis B Patients With Mildly Elevated Alanine Aminotransferase Jian Wang, Zhiyi Zhang, Li Zhu, Tao Fan, Ye Xiong, Shaoqiu Zhang, Chao Jiang, Shengxia Yin, Xin Tong, Juan Xia, Xiaomin Yan, Renling Yao, Yu Shi, Xingxiang Liu, Chuanwu Zhu, Chao Wu, Rui Huang Clinical Gastroenterology and Hepatology.2026;[Epub] CrossRef
Steatosis paradox: Unraveling pathways of suppressive effect of hepatic steatosis on hepatitis B virus Shang-Chin Huang, Jia-Horng Kao Biomedical Journal.2026; 49(3): 100969. CrossRef
Impact of Cardiometabolic Risk Factors and Steatotic Liver Disease on Liver‐Related Outcomes in Patients With Chronic Hepatitis C After Curative Antiviral Therapy Chung‐Feng Huang, Yi‐Hung Lin, Pei‐Chien Tsai, Ming‐Lun Yeh, Chih‐Wen Wang, Tyng‐Yuan Jang, Po‐Cheng Liang, Yu‐Ju Wei, Nai‐Jen Hou, Ming‐Yen Hsieh, Chao‐Kuan Huang, Tzu‐Chun Lin, Jee‐Fu Huang, Chia‐Yen Dai, Wan‐Long Chuang, Ming‐Lung Yu The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Absence of steatosis combined with cardiometabolic risk factors confers the highest hepatocellular carcinoma risk in treated chronic hepatitis B Hung-Wei Wang, Hsueh-Chou Lai, Wei-Fan Hsu, Sheng-Hung Chen, Yi-Chun Kuo, Cheng-Yuan Peng Annals of Medicine.2026;[Epub] CrossRef
Diagnosing and defining MASLD in people living with chronic hepatitis B Emily Martyn, Alejandro Arenas-Pinto, Richard Gilson, Nomathemba Chandiwana, Stuart Flanagan, Douglas MacDonald, Emmanuel A. Tsochatzis, W. D. Francois Venter, Jennifer Manne-Goehler, Philippa C. Matthews Communications Medicine.2026;[Epub] CrossRef
The Chronic Hepatitis B and Metabolic Dysfunction-Associated Steatotic Liver Disease Paradox: Friend or Foe? Shang-Chin Huang, Tai-Chung Tseng Gut and Liver.2026; 20(3): 350. CrossRef
Insulin Resistance and Hepatocellular Carcinoma Development in Chronic Hepatitis B Patients Under Antiviral Therapy Dong Hyun Sinn, Kyung-Ah Kim, Jung Il Lee, Geum-Youn Gwak Journal of Korean Medical Science.2026;[Epub] CrossRef
Differential HCC risk among HBV indeterminate types at baseline and by phase transition Rui Huang, Huy N Trinh, Satoshi Yasuda, Angela Chau, Mayumi Maeda, Ai-Thien Do, Daniel Q Huang, Takanori Ito, Takashi Honda, Masatoshi Ishigami, Ritsuzo Kozuka, Carmen Monica Preda, Cheng-Hao Tseng, Sebastián Marciano, Pei-Chien Tsai, Dong Hyun Lee, Chris Gut.2025; 74(11): 1873. CrossRef
Incidence and determinants of achieving HBsAg <100 IU/mL in HBeAg-negative CHB patients with nucleos(t)ide analogue treatment Jian Wang, Tao Fan, Zhiyi Zhang, Li Zhu, Shaoqiu Zhang, Ye Xiong, Chun Shan, Chao Jiang, Shengxia Yin, Xin Tong, Renling Yao, Juan Xia, Xiaomin Yan, Yu Shi, Yuxin Chen, Xingxiang Liu, Huali Wang, Haixia Zhang, Chuanwu Zhu, Qun Zhang, Chao Wu, Rui Huang Emerging Microbes & Infections.2025;[Epub] CrossRef
Impact of metabolic dysfunction on treatment responses to nucleos(t)ide analogues in chronic hepatitis B: a retrospective multi-center REAL-B cohort study Rui Huang, Dae Won Jun, Hidenori Toyoda, Yao-Chun Hsu, Huy Trinh, Akito Nozaki, Toru Ishikawa, Tsunamasa Watanabe, Haruki Uojima, Daniel Q. Huang, Takashi Honda, Yasuhito Tanaka, Philip Vutien, Sebastián Marciano, Hiroshi Abe, Masaru Enomoto, Masanori Ats eClinicalMedicine.2025; 87: 103407. CrossRef
Aspirin Use and Risk of HCC and Gastrointestinal Bleeding in Patients With HBV‐Related Cirrhosis: A Landmark Analysis Mi Na Kim, Geun U. Park, Seng Chan You, Jae Seung Lee, Hye Won Lee, Beom Kyung Kim, Seung Up Kim, Jun Yong Park, Do Young Kim, Sang Hoon Ahn Journal of Gastroenterology and Hepatology.2025; 40(11): 2750. CrossRef
Multifunctional Metal Composite Hydrogels for Diabetic Wound Therapy Shengnan Zhang, Hui Gao, Kevin H. Mayo, Jingang Mo, Le Deng Gels.2025; 11(12): 960. CrossRef
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
Metabolic dysfunction-associated steatotic liver disease and adverse pregnancy outcomes: a nationwide cohort study Young Mi Jung, Taesu Kim, Min-Jeong Oh, Dong Hyeon Lee, Geum Joon Cho, Won Kim Hepatology International.2026; 20(1): 69. CrossRef
Unmasking Kidney Risk in Steatotic Liver Disease: A Call for Metabolic Precision Chan-Young Jung Gut and Liver.2026; 20(1): 1. CrossRef
Prognostic value of non-invasive fibrosis assessment scores in predicting mortality among individuals with metabolic dysfunction-associated steatotic liver disease Lingjie Wu, Shunling Cai, Zhongbin Lin, Ruilie Chen, Yuanfeng Zhang, Xiaobing Gong BMC Public Health.2026;[Epub] CrossRef
Optimal screening criteria for metabolic dysfunction-associated steatotic liver disease with fibrosis Byeong Geun Song, Myung Ji Goh, Wonseok Kang, Geum-Youn Gwak, Yong-Han Paik, Moon Seok Choi, Joon Hyeok Lee, Dong Hyun Sinn Annals of Hepatology.2026; 31(2): 102199. CrossRef
Managing Metabolic Dysfunction–Associated Steatotic Liver Disease: Protocol for a Scoping Review of Patient Perceptions, Barriers, and Facilitators Sikyeong Park, Yu Shin Park, Dahye Hong, Bada Kang JMIR Research Protocols.2026; 15: e81404. CrossRef
Risk Stratification of Chronic Kidney Disease in Adults Using Noninvasive Fibrosis Tests Based on the American Diabetes Association Algorithm Chan‐Young Jung, Hye Won Lee, Jung Il Lee, Han Ah Lee, Seung Up Kim Diabetes, Obesity and Metabolism.2026; 28(6): 5240. CrossRef
Rethinking first-line screening in MASLD beyond the limitations of Fibrosis-4 index: Editorial on “Risk stratification by noninvasive tests in patients with metabolic dysfunction-associated steatotic liver disease” Han Ah Lee, Young Youn Cho, Hyung Joon Kim Clinical and Molecular Hepatology.2026; 32(2): 921. CrossRef
Metabolic Dysfunction‐Associated Steatotic Liver Disease and Obesity: Pathogenesis, Diagnostics, Risk Stratification, and Therapeutic Approach Beom Kyung Kim The Kaohsiung Journal of Medical Sciences.2026;[Epub] CrossRef
Metabolic dysfunction-associated steatotic liver disease: On track to become the dominant etiology of hepatocellular carcinoma: Reply to correspondence on “Downregulation of the MARC1 p.A165 risk allele reduces hepatocyte lipid content by increasing beta- Jian Xu, Wei Zhang, Guo Wu, Jingdong Li Clinical and Molecular Hepatology.2026; 32(2): e257. CrossRef
Current Trends and Perspectives on Obesity and Metabolic Dysfunction-Associated Steatohepatitis in East Asia Soo Lim, Hui Zhou, Wataru Ogawa Journal of Obesity & Metabolic Syndrome.2026; 35(2): 130. CrossRef
Evolving B-mode ultrasound-based techniques for assessing metabolic dysfunction-associated steatotic liver disease: Now and beyond Walaa Abdelhamed, Mohamed Elbadry, Mohamed El-Kassas Liver Research.2026; 10(2): 109. CrossRef
Baduanjin for Non-Alcoholic Fatty Liver Disease: A Systematic Review Hyo-Ju Woo, Jung-Gyung Lee, Bong-Jin Shin, Jae-Jin Han, Sun-Young Park, Eui-Hyoung Hwang Journal of Korean Medicine Rehabilitation.2026; 36(2): 85. CrossRef
Surgically confirmed severe endometriosis is associated with lower risk of steatotic liver disease: Evidence of estrogen‐linked hepatic–reproductive crosstalk Jung Hyun Park, Keungmo Yang, Hyun Yang, Si Hyun Bae, Mee‐Ran Kim, Jaejun Lee International Journal of Gynecology & Obstetrics.2026;[Epub] CrossRef
Non-Invasive Tests in the Management of Metabolic Dysfunction-Associated Steatotic Liver Disease: From Diagnosis to Treatment Monitoring Han Ah Lee, Young Youn Cho, Hyung Joon Kim Clinical Ultrasound.2026; 11(1): 1. CrossRef
An Arterial‐Enhancing Liver Nodule With Washout in a Patient With Metabolic and Alcohol‐Associated Liver Disease Soon Kyu Lee, Sun Young Jun, Young Chul Yoon Journal of Gastroenterology and Hepatology.2026; 41(7): 1991. CrossRef
Metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated alcohol-related liver disease in human immunodeficiency virus Dinuka Bandara, Krishan Joshi, Carol Singh, Aalam Sohal, Mohanad Al-Qaisi, Nilofar Najafian World Journal of Virology.2026;[Epub] CrossRef
CT attenuation–based hepatic steatosis assessment using 3D organ segmentation: Impact of tube voltage and need for cutoff adjustment Jeongin Yoo, Ijin Joo, Sun Kyung Jeon, Junghoan Park, Jeong Min Lee European Journal of Radiology.2026; 203: 113021. CrossRef
Alcohol consumption and dementia risk in steatotic liver disease: a nationwide cohort study Ji Won Han, Seunghee Na, Kyungdo Han, Kyu Na Lee, Do Young Kim, Sang Hoon Ahn, Mi Na Kim Hepatology International.2026;[Epub] CrossRef
Pharmacological treatment of metabolic dysfunction–associated steatotic liver disease: a narrative review Jeong-Hwan Lee, Jeong-Ju Yoo, Sang Gyune Kim, Young Seok Kim Journal of the Korean Medical Association.2026; 69(6): 492. CrossRef
Differential Infiltration of T-Cell Populations in Tumor and Liver Tissues Predicts Recurrence-Free Survival in Surgically Resected Hepatocellular Carcinoma Eun Ji Jang, Ho Joong Choi, Young Kyoung You, Deok Hwa Seo, Mi Hyun Kwon, Keungmo Yang, Jaejun Lee, Jeong Won Jang, Seung Kew Yoon, Ji Won Han, Pil Soo Sung Cancers.2025; 17(9): 1548. CrossRef
Metabolic Dysfunction-Associated Steatotic Liver Disease, Recent Revision of Terminology and Its Implications Hyo Young Lee, Eileen L. Yoon The Korean Journal of Gastroenterology.2025; 85(2): 126. 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
A Case Report of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) with Improved Cardiometabolic Risk Factors Following Treatment with Saenggangunbi-tang Eun Kyung Lee, Min Jeong Park, Youngchul Kim, Jang-Hoon Lee The Journal of Internal Korean Medicine.2025; 46(2): 303. CrossRef
Food Nutrients and Bioactive Compounds for Managing Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comprehensive Review Erdenetsogt Dungubat, Kohei Fujikura, Masahiko Kuroda, Toshio Fukusato, Yoshihisa Takahashi Nutrients.2025; 17(13): 2211. CrossRef
Associations between steatotic liver disease subtypes and incident atrial fibrillation in young adults: a nationwide cohort study Jeayeon Park, Goh Eun Chung, Su Jong Yu, Yoon Jun Kim, Jung-Hwan Yoon, Kyungdo Han, Eun Ju Cho Cardiovascular Diabetology.2025;[Epub] CrossRef
Second-line antidiabetic drugs: friend or foe of the liver Jiwon Yang, Gunho Kim, Ju Hyun Shim, Jihyun An Journal of Liver Cancer.2025; 25(2): 187. CrossRef
Extrahepatic manifestation of metabolic dysfunction-associated steatotic liver disease Anoushka Shenoy, Aijaz Ahmed, Donghee Kim Metabolism and Target Organ Damage.2025;[Epub] CrossRef
2025 Clinical Practice Guidelines for Diabetes: Management of Metabolic Dysfunction-Associated Steatotic Liver Disease Jaehyun Bae The Journal of Korean Diabetes.2025; 26(3): 172. CrossRef
Paired snRNA-seq and scRNA-seq analysis of MASLD patients to identify early-stage markers for disease progression Suebin Park, Su-Hyeon Lee, Se-eun Han, Beom Kyung Kim, Byungjin Hwang Hepatology Communications.2025;[Epub] CrossRef
Sex Hormones and Metabolic Dysfunction-Associated Steatotic Liver Disease Ralf Weiskirchen, Amedeo Lonardo International Journal of Molecular Sciences.2025; 26(19): 9594. CrossRef
Discovery of ultrasound-derived fat fraction as a non-invasive tool for MASLD diagnosis Huiru Jin, Mengfan Jiao, Chengxiao Yu, Tingting Ren, Qingling Chen, Zixing Dai, Erfu Xie, Longfeng Jiang, Yuwen Li European Journal of Medical Research.2025;[Epub] CrossRef
Risk of Esophageal and Gastric Cancer by Histologic Subtype in Steatotic Liver Disease: A UK Biobank Study Donghoon Kang, Ji Won Han, Kenneth R. Muir, Artitaya Lophatananon, Jongin Lee Cancers.2025; 17(21): 3416. CrossRef
Implication of the Androgen Receptor in Muscle–Liver Crosstalk: An Overlooked Mechanistic Link in Lean-MASLD Eleni Myrto Trifylli, Christiana Charalambous, Nikolaos Spiliotopoulos, Nikolaos Papadopoulos, Anastasia Oikonomou, Spilios Manolakopoulos, Melanie Deutsch Livers.2025; 5(4): 65. CrossRef
Time-updated FIB-4 index predicts coronary artery calcification progression in individuals with metabolic dysfunction–associated steatotic liver disease Yesung Lee, Woncheol Lee Scientific Reports.2025;[Epub] CrossRef