A paradigm shift in fatty liver disease nomenclature has introduced steatotic liver disease (SLD) as an umbrella term, encompassing metabolic dysfunction–associated steatotic liver disease (MASLD), metabolic dysfunction and alcohol-related liver disease (MetALD), and alcohol-associated liver disease (ALD). These SLD subtypes exist along a dynamic continuum shaped by the synergistic interplay of metabolic dysfunction and alcohol exposure. Accumulating evidence indicates that SLD exhibits distinct outcome-based clusters reflecting heterogeneity in pathogenic drivers and clinical trajectories. Cardiometabolic clusters, most prominently observed in MASLD, are characterized by systemic metabolic dysfunction and confer increased risks of cardiovascular disease (CVD). In contrast, liver-specific clusters demonstrate progressive fibrosis and cirrhosis, hepatic decompensation, and hepatocellular carcinoma. In large-scale cohorts, CVD accounts for 40-50% of deaths in MASLD, while liver-related mortality predominates in ALD (>60%). The relative dominance of cardiometabolic versus liver-specific clusters shifts progressively across the MASLD-MetALD-ALD spectrum. While CVD remains a major driver of mortality, particularly in MASLD, hepatic outcomes increase stepwise with advancing fibrosis and greater alcohol exposure. Advanced fibrosis is the predominant shared determinant amplifying both CVD and hepatic risks across subtypes. This review synthesizes cardiovascular and hepatic outcome patterns across the MASLD-MetALD-ALD spectrum, highlighting the prognostic reorientation across the continuum, in which hepatic outcomes rise stepwise with alcohol exposure while cardiovascular risk remains an important but less subtype-differentiated burden. These findings advocate outcome-oriented risk stratification integrating noninvasive fibrosis assessment, alcohol biomarkers (PEth), and cardiovascular risk calculators within the Cardiovascular-Kidney-Metabolic framework. Understanding SLD as a modifiable continuum enables individualized management to optimize multisystem outcomes.
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.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of hepatic decompensation and liver-related death, but most patients with MASLD do not develop these liver-related complications. Risk prediction and care pathways are crucial to identify which patients with MASLD are highest risk and link them to appropriate care. Risk prediction is usually done with blood-based algorithms such as Fibrosis-4 (FIB4), AST/platelet ratio index (APRI), and more recent scores such as steatotic-associated fibrosis estimator (SAFE) and LiverRisk Score. Second-line tests include Enhanced Liver Fibrosis (ELF) and imaging-based tests such as vibration-controlled transient elastography, shear wave elastography, or magnetic resonance elastography. We propose a consensus risk stratification care pathway that can be adapted for different clinical settings. We also discuss key needs to improve upon the state of the art: improving diagnosis/prognostic accuracy especially of blood-based models, optimizing calibration, and ensuring interpretability of predictive models. Finally, we discuss recent advances in clinical decision support systems including best practice advisories, dashboards, and dynamic guidelines. We highlight factors critical to clinical decision support systems including integration with existing systems and clinician workflows, minimizing additional burden to clinicians, provision of decision support and recommendations at the time/place of decision making, and continuous evaluation and local user involvement.
Hyun Ahm Sohn, Hanyong Go, Tae Hyeon An, Jun Min Lee, Hee-Jin Kim, Keeok Haam, Amal Magdy, Hyo-Jung Jung, Yang-Ji Shin, Hyun Jung Lim, Yujin Jeong, Yejin Bae, Youngae Jung, Seong-Hwan Park, Kyung Chan Park, Myeong Jun Song, Eun-Wie Cho, Eun-Soo Kwon, Jeong Hwan Park, Murim Choi, Geum-Sook Hwang, Dong Hyeon Lee, Stefano Romeo, Kyoung-Jin Oh, Won Kim, Mirang Kim
Received September 25, 2025 Accepted January 23, 2026 Published online January 27, 2026
Background/Aims Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide. Aberrant DNA methylation, which is primarily maintained by DNA methyltransferase 1 (DNMT1), has been linked to metabolic dysregulation; however, its contribution to MASLD pathogenesis remains poorly defined. This study aimed to elucidate the role of DNMT1-mediated methylation in transcriptional regulation during MASLD progression and to determine whether DNMT1 inhibition can reverse disease-associated epigenetic and transcriptional alterations.
Methods We conducted integrated analyses of the liver transcriptome (n = 131) and DNA methylome (n = 106) of patients with biopsy-proven MASLD. We evaluated the effect of DNMT1 inhibition with 5-aza-4′-thio-2′-deoxycytidine (Aza-TdC) on a diet-induced MASLD mouse model. Multiomics approaches, including DNA methylome profiling, lipidomics, bulk and single-nucleus RNA sequencing, and chromatin immunoprecipitation sequencing, were applied to elucidate the role of DNMT1-mediated DNA methylation in regulating pathogenic gene expression.
Results DNA methylome profiling revealed increased methylation variability associated with increased DNMT1 expression in MASLD patients. DNMT1 inhibition ameliorated dysregulated lipid metabolism by reducing hepatic triacylglycerol accumulation and inflammation. Aza-TdC treatment partially reversed MASLD-related hypermethylation of hepatocyte nuclear factor 4 alpha (HNF4α)- and peroxisome proliferator-activated receptor alpha (PPARα)-regulated genes, restoring their transcriptional activity. Notably, Aza-TdC reactivated the gluconeogenic enzyme-encoding gene phosphoenolpyruvate carboxykinase 1 (PCK1), which was hypermethylated and transcriptionally repressed in MASLD. Targeted DNA methylation of the PCK1 promoter using CRISPRoff confirmed the direct epigenetic regulation of PCK1 expression.
Conclusions Targeting DNMT1 may mitigate lipid dysregulation and inflammation by reversing hypermethylation and restoring HNF4α- and PPARα-dependent gene transcription, highlighting DNMT1 as a potential therapeutic target for MASLD.
Christian Brion, Stephen Aurelien Hoang, Guangliang Wang, Faridodin Mirshahi, Jessie Ang, Matthew Ray Long, Zheng Zhu, Bhanu Sakhamuri, Molly Anderson Srour, Mohammad Shadab Siddiqui, Amon Asgharpour, David John Hayes, Neal Charles Foster, David William Salzman, Arun Jayant Sanyal
Clin Mol Hepatol 2026;32(2):706-720. Published online December 26, 2025
Background/Aims MicroRNA (miRNA) isoforms (isomiRs) broaden the regulatory landscape of canonical miRNAs, but their role in metabolic dysfunction-associated steatotic liver disease (MASLD) remains unknown. We aimed to characterize the hepatic isomiR landscape in MASLD and define their association with disease activity and fibrosis.
Methods Small RNA (sRNA) sequencing was performed on liver biopsies from 79 patients across the histological spectrum of MASLD. IsomiRs were annotated and quantified. Their association to disease activity and fibrosis score was assessed by differential expression, ordinal regression, and machine learning. Parallel mRNA sequencing and pathway enrichment were used to map isomiR–mRNA interactions and regulatory networks, which were validated against an independent dataset.
Results MiRNAs accounted for 75% of sRNAs in liver tissue, of which 67% were isomiRs. Across MASLD severity, 173 isomiRs correlated with disease activity and 58 with fibrosis stage. Key findings included a miR-122 isomiR uniquely targeting INSIG1 (cholesterol metabolism) and a miR-21 isomiR targeting PPARA and HMGCS2 (lipid and fibrosis pathways). Integration with mRNA data revealed 33 dysregulated pathways, including PPAR signaling, insulin resistance, and TGF-β response. Several novel isomiRs from miR-26b, let-7c, and miR-32 families were also linked to lipid metabolism and fibrosis progression.
Conclusions IsomiRs represent the majority of hepatic miRNAs and uncover novel regulatory networks masked by canonical miRNA analysis. These findings provide new insights into the molecular heterogeneity of MASLD, highlight candidate pathways driving disease progression, and identify potential biomarkers and therapeutic targets for precision hepatology.
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The Role of MicroRNAs in the Progression of Metabolic Dysfunction-associated Steatotic Liver Disease Jang Hyun Choi Journal of Digestive Cancer Research.2026; 14(1): 82. 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;[Epub] CrossRef
Jonggi Choi, Daniel Fulop, Vy H. Nguyen, Eric Przybyszewski, Jiunn Song, Allison Carroll, Megan Michta, Erik Almazan, Tracey G. Simon, Raymond T. Chung
Clin Mol Hepatol 2026;32(1):305-317. Published online November 11, 2025
Background/Aims Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing cause of cirrhosis and its complications. Given its close association with type 2 diabetes mellitus (T2DM), evaluating whether sodium-glucose cotransporter-2 inhibitors (SGLT2is) can mitigate the progression of liver fibrosis is clinically important. We examined the association between SGLT2i use and liver fibrosis progression in patients diagnosed with MASLD and T2DM.
Methods We conducted a target trial emulation study using a retrospective, active comparator new-user design among adults with MASLD, T2DM, and low-to-intermediate Fibrosis-4 (FIB-4≤2.67) scores who initiated treatment with either SGLT2is or dipeptidyl peptidase-4 inhibitors (DPP-4is) at Mass General Brigham or Asan Medical Center from 2013 to 2023. The primary outcome was the progression to advanced fibrosis (FIB-4>2.67), confirmed on ≥2 occasions within 1 year. The secondary outcome was the development of major adverse liver outcomes (MALO), including incident cirrhosis, decompensation events, hepatocellular carcinoma, or liver transplantation.
Results Among 16,901 eligible patients, 2,571 propensity score-matched pairs were identified with balanced baseline characteristics. During follow-up (median, 3.7 years), fibrosis progression occurred at a rate of 3.46/100 personyears in SGLT2i users and 4.44 in DPP4i users. SGLT2i use was associated with a lower risk of fibrosis progression (HR 0.78, 95% CI 0.67–0.89; P<0.001). No significant difference in MALO incidence was observed. Subgroup analyses showed a consistent association among users of metformin, statins, and aspirin.
Conclusions SGLT2i use was associated with reduced risk of fibrotic progression compared to DPP4i use in adults with MASLD and T2DM.
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.
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Background/Aims Metabolic dysfunction-associated steatotic liver disease (MASLD) may progress to liver inflammation, fibrosis, cirrhosis and hepatocellular carcinoma. So far, genome-wide association studies explain a small fraction of MASLD heritability.
Methods We sought to identify novel genetic determinants of MASLD by exploring interactions between genetic variants and body mass index (BMI). First, we examined genome-wide interactions with BMI for circulating alanine aminotransferase (ALT) levels using UK Biobank data. For identified loci, we next examined associations with hepatic proton density fat fraction (PDFF) in 35,146 independent UK Biobank participants. Associations with PDFF were replicated in four independent European cohorts, followed by a phenome-wide association study. Finally, we used human liver epigenomic maps and CRISPR/Cas9 experiments in vitro and in vivo to functionally characterize the CYP7A1 locus.
Results Thirteen loci interact with BMI for ALT (P<5E-8), including eight well-known genetic modulators of MASLD. Two loci—UBXN2B/CYP7A1 and GIPR—are additionally associated with PDFF. For the intronic rs34783010 in GIPR, the minor T allele is associated with lower BMI and higher HbA1c and liver triglyceride content in humans. The UBXN2B/CYP7A1 locus is associated with PDFF in four additional European cohorts. Epigenomic data and in vitro experiments in human liver cells prioritise rs10504255 and CYP7A1 as the functional effectors in this locus. Perturbation of CYP7A1 orthologues using CRISPR/Cas9 results in less liver fat in 10-day-old, metabolically challenged zebrafish larvae.
Conclusions A genome-wide single nucleotide polymorphism×BMI design fuelled identification of two MASLD genes: CYP7A1 and GIPR.
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Background/Aims Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global epidemic. The disease has a strong genetic component, and a common missense variant (rs2642438) in the mitochondrial amidoxime-reducing component 1 (MARC1) gene confers protection against its onset and severity. However, there are contrasting results regarding the mechanisms that promote this protection.
Methods We downregulated MARC1 in primary human hepatocytes (PHHs) using short interfering RNA (siRNA). We measured neutral lipid content by Oil-Red O staining and fatty acid oxidation by radiolabeled tracers. We also performed RNA-sequencing and proteomic analysis using LC-MS. Additionally, we analyzed data from 239,075 participants from the UK Biobank.
Results Downregulation of MARC1 reduced neutral lipid content in PHHs homozygous for the wild type (p.A165, risk), but not for the mutant (p.T165, protective), allele. We found that this reduction was mediated by increased fatty acid utilization via β-oxidation. Consistent with these results, we found that the levels of 3-hydroxybutyrate, a by-product of β-oxidation, were higher in carriers of the rs2642438 minor allele among samples from the UK biobank, indicating higher β-oxidation in these individuals. Moreover, downregulation of the MARC1 p.A165 variant resulted in a more favorable phenotype by reducing ferroptosis and reactive oxygen species levels.
Conclusions MARC1 downregulation in carriers of the risk allele results in lower hepatocyte neutral lipids content due to higher β-oxidation, while upregulating beneficial pathways involved in cell survival.
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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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One-third of adults across the globe exhibit metabolic dysfunction-associated steatotic liver disease (MASLD)―formerly known as nonalcoholic fatty liver disease (NAFLD). To date, MASLD is the fastest-growing etiology of chronic liver disease and hepatocellular carcinoma (HCC). Besides the population with obesity, MASLD can also be found in lean populations, accounting for 13% of the global population, especially Asians. Notably, individuals with lean MASLD face equal or higher overall mortality rates compared to their non-lean counterparts. Risk modifiers encompass advanced age, hepatic fibrosis, and type 2 diabetes mellitus (T2DM). Moreover, the population with lean MASLD is associated with an increased risk of HCC, while their non-lean counterparts are more prone to cardiovascular outcomes and T2DM. Existing evidence indicates a similar risk of liver-related events and extrahepatic cancer between the two groups. However, MASLD-related genetic variants, such as PNPLA3 and TM6SF2, did not significantly affect mortality between the two populations. Still, underreporting alcohol consumption and regional representation limits the study’s comprehensiveness. Longitudinal studies and mechanistic explorations are needed to understand differences in lean versus non-lean MASLD populations. This review highlights the need for awareness and tailored interventions in managing MASLD, considering lean individuals’ unique risks.
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Background/Aims Evidence suggests that the gastrointestinal microbiome plays a significant role in the biology of metabolic dysfunction-associated steatotic liver disease (MASLD). However, it remains unclear whether disparities in the gut microbiome across intestinal tissular compartments between the sexes lead to MASLD pathogenesis.
Methods Sex-specific analyses of microbiome composition in two anatomically distinct regions of the gut, the small intestine and colon, were performed using an experimental model of MASLD. The study involved male and female spontaneously hypertensive rats and the Wistar-Kyoto control rat strain, which were fed either a standard chow diet or a high-fat diet for 12 weeks to induce MASLD (12 rats per group). High-throughput 16S sequencing was used for microbiome analysis.
Results There were significant differences in the overall microbiome composition of male and female rats with MASLD, including variations in topographical gut regions. The beta diversity of the jejunal and colon microbiomes was higher in female rats than in male rats (PERMANOVA p-value=0.001). Sex-specific analysis and discriminant features using LEfSe showed considerable variation in bacterial abundance, along with distinct functional properties, in the jejunum and colon of animals with MASLD. Significantly elevated levels of lipopolysaccharide and protein expression of Toll-like receptor 4 were observed in the livers of male rats with MASLD compared with their female counterparts.
Conclusions This study uncovered sexual dimorphism in the gut microbiome of MASLD and identified microbial heterogeneity within intestinal compartments. Insights into sex-specific variations in gut microbiome composition could facilitate customised treatment strategies.
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As the rates of obesity and type 2 diabetes (T2D) continue to increase globally, so does the prevalence of metabolic dysfunction–associated steatotic liver disease (MASLD). Currently, 38% of all adults and 7–14% of children and adolescents have MASLD. By 2040, the MASLD prevalence rate for adults is projected to increase to more than 55%. Although MASLD does not always develop into progressive liver disease, it has become the top indication for liver transplant in the United States for women and those with hepatocellular carcinoma (HCC). Nonetheless, the most common cause of mortality among patients with MASLD remains cardiovascular disease. In addition to liver outcomes (cirrhosis and HCC), MASLD is associated with an increased risk of developing de novo T2D, chronic kidney disease, sarcopenia, and extrahepatic cancers. Furthermore, MASLD is associated with decreased health-related quality of life, decreased work productivity, fatigue, increased healthcare resource utilization, and a substantial economic burden. Similar to other metabolic diseases, lifestyle interventions such as a heathy diet and increased physical activity remain the cornerstone of managing these patients. Although several obesity and T2D drugs are available to treat co-morbid disease, resmetirom is the only MASH-targeted medication for patients with stage 2–3 fibrosis that has approved by the Food and Drug Administration for use in the United States. This review discusses MASLD epidemiology and its related risk factors and outcomes and demonstrates that without further global initiatives, MASLD incidence could continue to increase.
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Assessment of the Diagnostic Performance and Clinical Impact of AI in Hepatic Steatosis: Systematic Review and Meta-Analysis Jiamei Song, Dan Liu, Jitong Li, Haoru Cong, Ruixue Deng, Yihan Lu, Jiayi Sun, Jingzhou Zhang Journal of Medical Internet Research.2026; 28: e78310. CrossRef
Semaglutide-Induced Weight Loss Is the Main Determinant for the Improvement of Hepatic Biochemistry and Elastographic Repeated Measurements with FibroScan® in Patients with Type 2 Diabetes Mellitus and Metabolic Dysfunction-Associated Steatotic Liver Dise Savvoula Savvidou, Elektra Augousti-Varela, Aikaterini Damianakou, Miltiadis Chalkias, Ioannis Stergiou Metabolic Syndrome and Related Disorders.2026; 24(3): 121. CrossRef
Oxidative stress in metabolic dysfunction-associated steatohepatitis: Mechanisms and emerging therapeutic strategies Yidan Chen, Hui Yu, Xinyu Kai, Runting Yin, Zhen Ouyang, Yuan Wei, Cai Zhang Biochemical Pharmacology.2026; 246: 117702. CrossRef
Diet intervention altered DNA methylation of potassium voltage-gated channel subfamily Q member 1 in metabolic dysfunction-associated steatohepatitis Xinyu Shi, Hualing Song, Xinying Xiong, Shuang Wei, Lei Zhang, Shengfu You, Wenjun Zhou, Guang Ji, Baocheng Liu, Na Wu Clinical Epigenetics.2026;[Epub] CrossRef
Mechanisms of scramblases in regulating hepatic lipoprotein secretion and autophagy Allen Chen, Chen Zhang, Wen-Xing Ding, Hong-Min Ni Journal of Lipid Research.2026; 67(2): 100979. CrossRef
Artificial Intelligence for Fibrosis Diagnosis in Metabolic-Dysfunction-Associated Steatotic Liver Disease: A Systematic Review Neilson Silveira de Souza, Théo Cordeiro Veiga Vitório, Raphael Augusto de Souza, Marcos Antônio Dórea Machado, Helma Pinchemel Cotrim Diagnostics.2026; 16(2): 261. CrossRef
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
Diagnostic Utility of Serum Activating Transcription Factor 4 and Toll-like Receptor 4 as Early Biomarkers of Inflammation in Metabolic Dysfunction–Associated Steatotic Liver Disease Isa Yalcinkaya, Iskender Ekinci, Seyma Dumur, Eda Nur Duran, Hafize Uzun, Melda Yalcinkaya, Elif Kadioglu Yeniyurt, Omer Vehbi Alpaydin, Gulden Anataca, Omur Tabak Journal of Clinical Medicine.2026; 15(2): 559. CrossRef
Use of Artificial Intelligence-Assisted Histopathology for Evaluation of Sex-Specific Progression and Regression of Hepatocellular Carcinoma Related to Metabolic Dysfunction-Associated Fatty Liver Disease Ke Yin, Yuyun Song, Ran Fei, Xu Cong, Baiyi Liu, Zilong Wang, Xin Ai, Minjun Liao, Yayun Ren, Kutbuddin Akbary, Wei Wang, Qiang Yang, Xiao Teng, Nan Wu, Huiying Rao, Xiaoxiao Wang, Feng Liu Diagnostics.2026; 16(2): 234. CrossRef
Effect of SGLT-2 inhibitors on liver fibrosis progression in patients with MASLD: an updated meta-analysis based on RCTs Lei Yang, Jiale Ruan, Yingying Fang, Anyi Xu Frontiers in Medicine.2026;[Epub] CrossRef
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
Phosphatidylserine Supplementation Improves Metabolic Liver Disease and Glycemic Control in the Presence of Suppressed Oxidative Glucose Metabolism Li Dong, Sihan Lin, John Slavin, Satya Gunnam, Zhili Cheng, Shuai Nie, Michael G. Leeming, Nicholas A. Williamson, Magdalene K. Montgomery Diabetes.2026; 75(2): 273. CrossRef
Integrating multi-omics and machine learning systematically deciphers cellular heterogeneity and fibrotic regulatory networks in the progression from MASLD to MASH Weiheng Wen, Zenghui Liu, Wenliang Tan, Yingzheng Tan, Wei Li, Jian Wan, Hongsai Hu, Zhengwu Jiang, Xing Tang, Jing Yang, Jiao Xiao, Xiongjin Tan, Xun Chen, Peili Wu, Yukun Li npj Digital Medicine.2026;[Epub] CrossRef
Morphological characterization of a novel model of steatohepatitis in the
FAH
-/-
pig
Silvana N. Wilken, Philipp Felgendreff, Anna Minshew, Boyukkhanim Ahmadzada, Seyed M. Hosseiniasl, Sara Kazeminia, Kachi Ezenekwe, Ameya Patil, Byoung U. Park, Ahmer Sultan, Lindsey Smith, Julio Cisneros Correa, Kamal Hussein, Harmeet Malhi, Roger K. More Veterinary Pathology.2026;[Epub] CrossRef
Association of cholesterol, high-density lipoprotein and glucose (CHG) index with mortality risk in metabolic dysfunction-associated steatotic liver disease (MASLD) adults: results from two prospective cohorts Huangxin Zhu, Lihua Liu, Sicheng Yang, Yunfeng Fu, Yating Pan, Qingan Fu, Fan Du, Xiaodong Zhou Cardiovascular Diabetology.2026;[Epub] CrossRef
Stemness CD24 activation promotes hepatocellular carcinoma progression via an immune escape mechanism Yin Cai, Lu-Yin Liu, Xiao-Xiao Xia, Hao Tang, Min Xu, Wen-Li Sai, Deng-Fu Yao, Min Yao World Journal of Gastroenterology.2026;[Epub] CrossRef
Targeting the 4-HNE–H₂S pathway as a therapeutic strategy for placental injury in pregnancy with MAFLD Tianxiao Hu, Jiayu Qi, Yinuo Xu, Jia He, Qingying Tan, Jie Hao, Jing Wang, Jiewei Hong, Jianwei Wang, Lin Chen, Xiaobing Dou International Immunopharmacology.2026; 172: 116245. CrossRef
Association of the Triglyceride-Glucose Index With Established Cardiovascular Disease in Adults With Metabolic Dysfunction-Associated Steatotic Liver Disease: A Cross-Sectional Study Soumayan Mondal, Sidharth S Pattnaik, Nihar Ranjan Mohanty, Sailendra Nayak, Ambika Mohanty, Shubhransu Patro Cureus.2026;[Epub] CrossRef
Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk Qiqi Zhao, Shengwen Lu, Yu Guan, Zhiwen Sun, Shi Qiu, Aihua Zhang Lipids in Health and Disease.2026;[Epub] 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
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Association Between Metabolically Associated Steatotic Liver Disease (MASLD) and Cardiovascular Risk Scores in Urban Adults FARIS HUSSAIN, KELVIN KANAYO NWABUEZE, FATIMA IJAZ, SONIA OUTALEB, MAHMUDUL HASAN NAHID, SYED ABID, MARIAM SALEEM, KHANT NYI ZAYA, SAIFULLAH SYED, HUMAIRA JANANTH, MANAHIL ZARIEF Juntendo Medical Journal.2026; 72(1): 54. CrossRef
Metabolic dysfunction-associated steatotic liver disease in patients with type 2 diabetes mellitus in Tanzania: prevalence and predictors Evangelista Malindisa, Illuminata Kafumu, Allen Rweyendera, Elisha Mkemangwa, David Majinge, Igembe Nkandala, Paulina Manyiri, Semvua Kilonzo BMC Endocrine Disorders.2026;[Epub] CrossRef
Body mass index and metabolic dysfunction associated steatotic liver disease remission among Chinese adults in a retrospective cohort study Jiwen Zhang, Yuyin Guo, Bi’e Li, Jiaqian Zhu, Chuang Gao, Qiongdan Zhang, Yong Han, Chuxuan Gu Scientific Reports.2026;[Epub] CrossRef
12,13-diHOME ameliorates MASLD by regulating Sestrin2-mediated AMPK/ULK1/Lipophagy in obese mice Kexin Zhang, Chengxia Kan, Hongyan Qiu, Junfeng Shi, Jian Chen, Tianpeng Zheng, Jingwen Zhang, Yujie Ma, Sufang Sheng, Ningning Hou, Fang Han, Xiaodong Sun Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease.2026; 1872(4): 168186. CrossRef
Burden of MASLD and liver fibrosis: evidence from Phenome India cohort Meghana Arvind, Anshul Verma, Sreeshma Raj K, Satyartha Prakash, Vignesh S. Kumar, Mohammad Azhar Uddin, Ayushi Narayan, Mamta Rathore, Nancy Rawat, Ankita Sahu, Yogesh Kumar, Pulkit Hasmukhbhai Leuva, Monika Sharma, Rajesh S, Dwaipayan Saha, Ankita Mridh The Lancet Regional Health - Southeast Asia.2026; 45: 100723. CrossRef
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Interactions Between the Gut Microbiome and Genetic and Clinical Risk Factors for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Patients with Type 2 Diabetes Mellitus from Different Geographical Regions of Argentina Bárbara Suarez, Adriana Mabel Álvarez, María Florencia Mascardi, Ana Laura Manzano Ramos, Dong Hoon Woo, María Mercedes Gutiérrez, Guillermo Alzueta, María del Carmen Basbus, Santiago Bruzone, Patricia Cuart, Guillermo Dieuzeide, Teresita García, Olga Esc Life.2026; 16(2): 283. CrossRef
Can ammonia scavenging treat MASLD? Evaluating the evidence for L‐ornithine L‐aspartate—A systematic review Abdulrahman Ismaiel, Vera Ciornolutchii, Stefan‐Lucian Popa, Dan L. Dumitrascu European Journal of Clinical Investigation.2026;[Epub] CrossRef
Predictive factors of metabolic dysfunction associated steatotic liver disease (MASLD) among individuals with cardio-metabolic risk factors, multicenter cross-sectional study, North East Ethiopia Getachew Bizuneh Aydagnuhm, Aklile Semu Tefera, Gebru Tesfaw Getahun, Ermiyas Endewunet Melaku BMC Gastroenterology.2026;[Epub] CrossRef
Temporal trends and racial/ethnic disparities in hepatocellular carcinoma incidence in the US between 2000-2022 Wenzhan Jing, Hang Pham, Samuel So JHEP Reports.2026; 8(4): 101754. CrossRef
Pirfenidone as a Pleiotropic Antifibrotic Agent in Metabolic Steatohepatitis: From Mechanisms to Clinical Evidence Mariana M. Ramírez-Mejía, Guadalupe Ponciano-Rodríguez, Jorge L. Poo, Nahum Méndez-Sánchez Archives of Medical Research.2026; 57(4): 103387. CrossRef
Long-term dementia risk in metabolic dysfunction-associated steatotic liver disease: a population-based study Andreas Bartholdy, Kristine Frøsig Moseholm, Pernille Yde Nielsen, Nicolai J. Wewer Albrechtsen, Lise Lotte Gluud, Majken Karoline Jensen Metabolic Brain Disease.2026;[Epub] CrossRef
Outils diagnostiques de la fibrose hépatique dans la stéatohépatite dysmétabolique Candice Gea, Guillaume Feugray, Valéry Brunel Revue Francophone des Laboratoires.2026; 2026(579): 36. CrossRef
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Noninvasive Testing for Metabolic Dysfunction-Associated Steatohepatitis (MASH) and Fibrosis Markos Kalligeros, Laurent Castera, Emmanuel A. Tsochatzis, Naim Alkhouri Clinics in Liver Disease.2026;[Epub] CrossRef
La ballonisation hépatocytaire : une nouvelle cible thérapeutique dans la Physiopathologie de la MASH Arthur Cens, Bart Staels, Réjane Paumelle Revue Francophone des Laboratoires.2026; 2026(579): 28. CrossRef
Febuxostat Improves MASLD in Male Rats: Roles of XOR Inhibition and Associated JNK/NRF2/HO-1 Pathway Changes Zhiyu Pu, Yangyang Cen, Bowen Yang, Kaijun Xing, Linxi Lian, Xi Chi, Jianjun Yang, Yannan Zhang International Journal of Molecular Sciences.2026; 27(2): 1069. CrossRef
Association between blood heavy metal levels and subtypes of steatotic liver disease: A nationally representative cross-sectional analysis in South Korea Ji Hye Choi, Juyeong Kim, Yesol Yim, Hyunjee Kim, Jiyoung Hwang, Ho Geol Woo, Sang Youl Rhee, Yerin Hwang, Dong Keon Yon Medicine.2026; 105(4): e47365. CrossRef
Biological aging across the metabolic dysfunction–associated steatotic liver disease spectrum: A systematic review Chukwuemeka E. Ogbu, Stella C. Ogbu, Chidera P. Ogbu, Chinazor Umerah iLIVER.2026; 5(1): 100222. CrossRef
Fermented Foods and the Gut–Liver Axis: Modulation of MASLD Through Gut Microbiota Agnieszka Wesołek-Leszczyńska, Dawid Rosiejka, Kalina Bogdańska, Paweł Bogdański Nutrients.2026; 18(3): 542. CrossRef
Association of four insulin resistance indices with liver‐related adverse outcomes: A prospective cohort study Xiao‐Meng Wang, Hao Yan, Wen‐Fang Zhong, Jia‐Hao Xie, Huan Chen, Jun‐Jie Wang, Wei‐Qi Song, Dong Shen, Pei‐Dong Zhang, Xi‐Ru Zhang, Jiao‐Jiao Ren, Dan Liu, Zhi‐Hao Li, Chen Mao Diabetes, Obesity and Metabolism.2026; 28(5): 3598. CrossRef
Efficacy of empagliflozin in patients with metabolic dysfunction-associated steatotic liver disease with or without diabetes: a systematic review and meta-analysis of randomized controlled trials Khalid I. AlHussaini Frontiers in Medicine.2026;[Epub] CrossRef
Association of Metabolic Dysfunction-Associated Steatotic Liver Disease with Extrahepatic Cancers and Sarcopenia Yusuf Yilmaz, Alina M. Allen, Jérôme Boursier, Juan P. Arab Clinics in Liver Disease.2026;[Epub] CrossRef
Associations of relative fat mass with metabolic dysfunction–associated steatotic liver disease and liver fibrosis: evidence from the U.S. NHANES 2017–2023 Hai-Yuan Zhong, Ling-Dan Ma, Jin-Cheng Li, Dan Jiang, Yu-Mei Qin, Ming-Yu Lai, Guang Xiong BMC Gastroenterology.2026;[Epub] CrossRef
Gut microbiota, liver disease, and perioperative anesthesia: interactions, risks, and therapeutic opportunities Lei Shi, Ye Yu, Zihan Ma, Weiyi Jiang Frontiers in Cellular and Infection Microbiology.2026;[Epub] CrossRef
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SIRT3 ameliorates hepatic inflammation, oxidative stress, and fibrosis in HFD- or MCD diet-fed mice Huifang Lv, Wenyue Sun, Cuixia Tian, Chunyong Bian, Zhongting Lu, Xin Guo The Journal of Nutritional Biochemistry.2026; 152: 110276. CrossRef
Paulobutalipin, a Lipid Accumulation Inhibitor from a Streptomyces sp. Thanh-Hau Huynh, Hoseo Lee, Sangwook Kang, Jeong-Hyeon Kim, Huiyeong Ju, Ki-Bong Oh, Sang-Jip Nam, Ja Hyun Koo, Dong-Chan Oh Journal of Natural Products.2026; 89(2): 682. CrossRef
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Polyunsaturated fatty acids as a potential preventive and therapeutic intervention for metabolic dysfunction–associated steatotic liver disease and its progression to hepatocellular carcinoma Thomai Kouti, Panayiota Christodoulou, Stephanos Christodoulides, Foula Protopapa, Charalambos Michaeloudes, Paraskevi A. Farazi Frontiers in Nutrition.2026;[Epub] CrossRef
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The active components of the Danshen-Shanzha herb-pair exert a protective effect on MASLD by synergistically promoting fatty acid oxidation via the activation of PPARα, Plin-5 and Plin-2 Ying Yang, Yaxing Li, Zirong Zhou, Hui Li, Yihan Ma, Wenjie Bi, Mengjiao Li, Xiaoli Liu, Qiang Jia, Liwen Han, Songsong Wang Journal of Ethnopharmacology.2026; 362: 121374. CrossRef
Efficacy and Safety of Statins in MASLD and Other Chronic Liver Diseases I. Commins, D. Clayton-Chubb, N. Janko, A. Majeed, W. Kemp, S. K. Roberts Medical Sciences.2026; 14(1): 84. CrossRef
Detection of hepatic steatosis with ultrasound-guided attenuation parameter (UGAP) in metabolic dysfunction-associated steatotic liver disease (MASLD) compared with proton density fat fraction (PDFF): Impact of measurement number and region of interest (R Marie Byenfeldt, Christer Grönlund, Patrik Nasr, Anna Lindam, Mattias Ekstedt, Peter Lundberg, Johan Kihlberg Ultrasound.2026;[Epub] CrossRef
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Efficacy of ursodeoxycholic acid in metabolic dysfunction-associated steatotic liver disease: an umbrella review of meta-analyses on liver enzymes Alsu R. Khurmatullina, Dmitrii N. Andreev, Igor V. Maev, Andrey V. Zaborovsky, Yury A. Kucheryavyy, Petr A. Beliy, Philipp S. Sokolov Frontiers in Medicine.2026;[Epub] CrossRef
Panax notoginseng Saponins Ameliorate High‐Fat Diet‐Induced Liver Injury via Mechanisms Involving TLR4‐Mediated Signaling and Lipid Metabolism Rong Li, Junyu Ma, Mengyao Li, Bangzhao Zeng, Xuexun Li, Xiaoyan Bi, Xin Zhao, Qin Gao, Yanling Yao, Yang Jiang, Chunmei Zhang, Fuli Ya Food Science & Nutrition.2026;[Epub] CrossRef
MicroRNA-146a Protects against Hepatocellular Carcinoma through Suppression of CCL5 Morgan C. Nelson, Liam C. O’Malley, Soh-Hyun Lee, Kaylyn M. Bauer, Arevik Ghazaryan, William W. Tang, Chad VanSant-Webb, Van B. Tran, Colton Hernandez, Ben Battistone, Amber Thibeaux, June L. Round, Micah J. Drummond, H. Atakan Ekiz, Kimberley J. Evason, Cancer Research Communications.2026; 6(2): 359. CrossRef
Imaging in MASLD Sudhakar K. Venkatesh Expert Review of Gastroenterology & Hepatology.2026; 20(3): 257. CrossRef
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Occurrence and prognosis of metabolic dysfunction-associated steatosis liver disease and gastrointestinal tumors: a systematic review and meta-analysis Siyu Duan, Yiyi Wei, Zhuoyu Ding, Chaomin Pan, Li Yang, Yan Gu, Xinke Wang PeerJ.2026; 14: e20616. CrossRef
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Altered Tryptophan–Kynurenine Pathway and Low-Grade Inflammation in Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD): Insights from LC–MS/MS–Based Metabolite Profiling Kübranur Ünal, Leyla İbrahimkhanlı, Mehmet Emre Erol, Nemat İbrahimkhanlı, Sabri Engin Altıntop, Mahi Nur Cerit, Ethem Turgay Cerit, Halit Nahit Şendur International Journal of Tryptophan Research.2026;[Epub] CrossRef
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Impact of different subtypes of steatotic liver disease on immune checkpoint inhibitor-related drug-induced liver injury: a retrospective study Tianyi Ma, Zhanfang Guo, Haijia Bi, Huawei Yuan, Yu Li, Mei Sun European Journal of Gastroenterology & Hepatology.2026; 38(3): 351. CrossRef
Triglyceride glucose index—a body shape index (TyG-ABSI) outperforms traditional obesity indices in predicting all-cause and cardiovascular mortality in metabolic-dysfunction associated steatotic liver disease: the mediating role of biological aging Guodong Yang, Wenli He, Xin Qiu, Shuang Shen, Peishu Li, Yifei Feng, Jiayuan Zhang, Bangde Xiang Cardiovascular Diabetology.2026;[Epub] CrossRef
The relationship between acromegaly and hepatic steatosis: insights from FibroScan imaging Tugce Apaydin, Haluk Tarik Kani, Caglayan Keklikkiran, Yusuf Yilmaz, Dilek Gogas Yavuz Journal of Endocrinological Investigation.2026; 49(5): 1029. CrossRef
From Childhood to Old Age: Current Knowledge and Practical Approaches to Metabolic Dysfunction-Associated Steatotic Liver Disease Iwona Gorczyca-Głowacka, Michał Tarnowski, Anna Zmelonek-Znamirowska, Przemysław Wolak Journal of Clinical Medicine.2026; 15(4): 1536. CrossRef
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Fecal microbiota transplantation alleviates steatosis and inflammation in high-fat and high-sugar diet-induced fatty liver in mice Fangxia Mi, Jinglu Guo, Wentao Zheng, Jianwei Shen, Hua Ye Frontiers in Cell and Developmental Biology.2026;[Epub] CrossRef
Coagulation protease-activated receptor-2 (PAR2) promotes dyslipidemia, obesity and MASLD through repression of the hepatic pioneer factor HNF4α Xinru Chen, Nga Nguyen, Susan E. Turner, Albert K. Tai, Manal F. Abdelmalek, Lidija Covic, Athan Kuliopulos JHEP Reports.2026; 8(6): 101796. CrossRef
Real-world comparison of GLP-1 agonists versus physical activity in metabolic dysfunction-associated steatotic liver disease Jason N. Chen, Bulent Tolga Delibasi, James Wang, Thomas Tran, Connie Hu, Charles W. Randall BMC Gastroenterology.2026;[Epub] CrossRef
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Using an integrative multi-omics and in vitro approach to investigate the role of tris(2-butoxyethyl) phosphate in promoting hepatic steatosis Gang Zhou, Xihan Gu, Xinyao Zhou, Shuai Chen, Hanyang Liu, Jing Wang BMJ Open Gastroenterology.2026; 13(1): e002123. CrossRef
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Alcohol-driven phenotypic transition in MASLD and risk of liver-related events Seohui Jang, Jihun Song, Eun Seok Kang, Sangwook Cheon, Taeho Kwak, Yihyun Kim, Seokjin Kong, Jinhyeok Choi, Minjeong Kang, Jaewon Khil, Hye Jun Kim, Jeongin Lee, Hwamin Lee, Seogsong Jeong JHEP Reports.2026; : 101866. CrossRef
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Role of MicroRNAs in Precision Hepatology Youngwoo Lee, Eunho Choi, Young-Sun Lee Journal of Digestive Cancer Research.2026; 14(1): 102. CrossRef
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
Bupleuri Radix ameliorates MASLD induced by high-fat diet and circadian disruption in rats: Involvement of the NR1D1–SREBF1/CYP7A1 circadian–metabolic axis Shuheng Wang, Shuaidong Bai, Tianhui Zhou, Yukun Wang, Xue Bai, Yiming Wang, Junwen Ma, Xuemei Qin, Xiaoxia Gao Journal of Ethnopharmacology.2026; 367: 121770. CrossRef
Comment on “High-normal and abnormal alanine transaminase levels linked to increased risk of hepatoma following treatment for chronic hepatitis C” Wen-Rui Li Journal of the Formosan Medical Association.2026;[Epub] CrossRef
Calorie Restriction Mitigates Steatotic Liver Disease in Obese Rats After Bariatric Surgery Yu-Ning Lin, Chin-Ying Wu, Yin-Ru Hsieh, Yi-Tung Lin, Weu Wang, Chun-Chao Chang, Shih-Yi Huang, Wei-Yu Kao Nutrition Research.2026;[Epub] CrossRef
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Familial hypobetalipoproteinemia in pediatric patients with fatty liver: an under-recognized cause Nurit Loberman Nachum, Eyal Shteyer, Hofit Cohen, Odelia Chorin, Maya Granot, Batia Weiss Frontiers in Medicine.2026;[Epub] CrossRef
The effect of a two-week low glycaemic index, higher fibre diet versus high glycaemic index diet on body composition, ectopic lipids, inflammatory biomarkers, gastrointestinal hormones and gut microbiota in metabolic dysfunction-associated steatotic liver Amina A. Al-Awadi, Jane I. Grove, Stephen Bawden, Amrita Vijay, Ana M. Valdes, Penny Gowland, Moira A. Taylor, Guruprasad P. Aithal Clinical Nutrition ESPEN.2026; 73: 103306. CrossRef
Di(2-ethylhexyl) phthalate exposure: Association with metabolic associated steatotic liver disease and underlying mechanisms Dapeng Yin, Yan Li, Wei Wu, Jiacheng Cheng, Xiaojuan Wang, Junhua He, Yikun Zhu, Jin Li Ecotoxicology and Environmental Safety.2026; 317: 120210. 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
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The Role of MicroRNAs in the Progression of Metabolic Dysfunction-associated Steatotic Liver Disease Jang Hyun Choi Journal of Digestive Cancer Research.2026; 14(1): 82. CrossRef
GCSH promotes MASH progression by regulating cuproptosis through the glycine–GSH metabolic pathway Xuan Fu, Yunmeng Li, Jing Chen, Baolong Yin, Mahbuba Nasrin, Rui Huo, Shuxin Tian Free Radical Biology and Medicine.2026; 252: 1. CrossRef
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Clinical differentiation between alcohol-associated and metabolic dysfunction-associated steatotic liver disease: a comparative case report Chang-Gue Son The Journal of Internal Korean Medicine.2026; 47(1): 70. CrossRef
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Background/Aims Steatotic liver disease (SLD) is a common manifestation in chronic hepatitis C (CHC). Metabolic alterations in CHC are associated with metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to elucidate whether hepatitis C virus (HCV) eradication mitigates MASLD occurrence or resolution.
Methods We enrolled 5,840 CHC patients whose HCV was eradicated by direct-acting antivirals in a nationwide HCV registry. MASLD and the associated cardiometabolic risk factors (CMRFs) were evaluated at baseline and 6 months after HCV cure.
Results There were 2,147 (36.8%) patients with SLD, and 1,986 (34.0%) of them met the MASLD criteria before treatment. After treatment, HbA1c (6.0% vs. 5.9%, P<0.001) and BMI (24.8 kg/m2 vs. 24.7 kg/m2, P<0.001) decreased, whereas HDL-C (49.1 mg/dL vs. 51.9 mg/dL, P<0.001) and triglycerides (102.8 mg/dL vs. 111.9 mg/dL, P<0.001) increased significantly. The proportion of patients with SLD was 37.5% after HCV eradication, which did not change significantly compared with the pretreatment status. The percentage of the patients who had post-treatment MASLD was 34.8%, which did not differ significantly from the pretreatment status (P=0.17). Body mass index (BMI) (odds ratio [OR] 0.89; 95% confidence intervals [CI] 0.85–0.92; P<0.001) was the only factor associated with MASLD resolution. In contrast, unfavorable CMRFs, including BMI (OR 1.10; 95% CI 1.06–1.14; P<0.001) and HbA1c (OR 1.19; 95% CI 1.04–1.35; P=0.01), were independently associated with MASLD development after HCV cure.
Conclusions HCV eradication mitigates MASLD in CHC patients. CMRF surveillance is mandatory for CHC patients with metabolic alterations, which are altered after HCV eradication and predict the evolution of MASLD.
Citations
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