Clinical and Molecular Hepatology最新文献

{"title":"GLP-1 receptor agonists and adverse outcomes in patients with type 2 diabetes and chronic viral hepatitis.","authors":"Xinrong Zhang, Xianhua Mao, Scott Barnet, Ramsey Cheung, Mindie H Nguyen","doi":"10.3350/cmh.2026.0746","DOIUrl":"https://doi.org/10.3350/cmh.2026.0746","url":null,"abstract":"<p><strong>Background/aims: </strong>Glucagon-like peptide-1 receptor agonists (GLP-1RA) are a novel class of anti-diabetic drugs that can treat obesity and type 2 diabetes (T2D). T2D and chronic viral hepatitis (CVH) frequently coexist and worsen liver and non-liver outcomes, but effective pharmacological therapies are limited. We aimed to evaluate the effect of GLP-1RA on liver and non-liver complications among patients with T2D and CVH in the United States.</p><p><strong>Methods: </strong>Patients with T2D and CVH initiating GLP-1RA were included (2013-2022) in Merative™ Marketscan® Research Databases. Primary outcomes included (1) hepatocellular carcinoma (HCC) and cirrhosis, and (2) cardiovascular disease (CVD), chronic kidney disease (CKD), and non-liver cancer. Cox proportional hazards models were conducted to estimate hazard ratio (HR) and 95% confidence interval (CI).</p><p><strong>Results: </strong>A total of 9,499 patients with T2D and CVH were included after 1:4 propensity score matching. Compared with non-GLP-1RA (N=7,366), GLP-1RA use (N=2,133) was associated with significantly lower risks of any liver-related outcomes (HR 0.71, 95% CI 0.57-0.87; P=0.001), HCC (HR 0.53, 95% CI 0.31-0.93; P=0.028), cirrhosis (HR 0.70, 95% CI 0.56-0.86; P<0.001), CKD (HR 0.67, 95% CI 0.53-0.84; P<0.001). A trend toward a lower risk of CVD (HR 0.82, 95% CI 0.66-1.03; P=0.089) and non-liver cancer (HR 0.73, 95% CI 0.53-1.01; P=0.055) was observed among GLP-1RA users, although the association did not reach statistical significance.</p><p><strong>Conclusions: </strong>GLP-1RA use was associated with lower risks of cirrhosis, HCC, and CKD among patients with T2D and CVH, with nonsignificant trends toward lower risks of CVD and non-liver cancer.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149263491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP22-mediated phagocytic evasion promotes immune escape in TP53-inactivated hepatocellular carcinoma.","authors":"Qifan Zhan, Qiaonan Shan, Jianan Xiang, Shengju Xu, Jiapei Wang, Jiongjie Yu, Guangjiang Jiang, Mingwei Gao, Shuqi Cai, Qianwei Ye, Chenyang Zhou, Nasha Qiu, Lu Yin, Mingcheng Wan, Tingting Feng, Haiyang Xie, Zi Yin, Rui Shao, Yishan Chen, Leiming Chen, Nan Wang, Jimin Liu, Wei Zhang, Yiren Hu, Zhe Tang, Shusen Zheng, Lixing Zhan, Xiao Xu, Sunbin Ling","doi":"10.3350/cmh.2026.0891","DOIUrl":"https://doi.org/10.3350/cmh.2026.0891","url":null,"abstract":"<p><strong>Background/aims: </strong>Hepatocellular carcinoma (HCC) is characterized by an immunosuppressive tumor microenvironment. Here, we aimed to elucidate the tumor cell-intrinsic functions of ubiquitin-specific protease 22 (USP22) in the immune escape of HCC cells.</p><p><strong>Methods: </strong>Autochthonous mouse models of HCC with either genetic Usp22 loss or Trp53 knockdown were used. In vitro and in vivo phagocytosis assays were performed to evaluate the interactions between HCC cells and macrophages. Multicolor fluorescence, spatial transcriptomics, immunoprecipitation and ubiquitination assays were used to explore the potential underlying mechanisms.</p><p><strong>Results and conclusions: </strong>We observed that tumor cell-intrinsic USP22 inhibits the infiltration and anticancer function of tumoricidal macrophages in HCC. USP22 expression in HCC cells blocks their direct phagocytosis by tumoricidal macrophages. Mechanistically, CD24 (a known phagocytosis checkpoint) mediates USP22-induced suppression of phagocytosis. USP22 promotes the transcriptional expression of CD24 by deubiquitinating and stabilizing the transcription factor E2F7. Furthermore, wild-type p53 downregulates USP22 protein expression, whereas TP53 inactivation markedly upregulates USP22 protein expression. The USP22-E2F7-CD24 axis is responsible for mediating TP53-inactivation-induced phagocytic evasion and hepatocarcinogenesis. Mechanistically, USP22 proteins bind to one another and suppress ubiquitination at the K442 residue. The wild-type p53 protein disrupts this mutual deubiquitination, thereby facilitating USP22 degradation. Moreover, TNF secreted by tumoricidal macrophages promotes USP22 degradation by disrupting its self-stabilizing mechanism in a wild-type p53-dependent manner. Our findings indicate that USP22-E2F7-CD24 axis-mediated phagocytic evasion promotes immune escape in TP53-inactivated HCC.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149263559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunotherapy and targeted therapy plus hepatic arterial infusion chemotherapy for HCC with portal vein tumor thrombosis (CHANCE2504): a nationwide target trial emulation study.","authors":"Long-Wang Lin, Qian Chen, Jia-Wei Zhou, Zhen Li, Bin Xiong, Jian-Song Ji, Xiao-Li Zhu, Bin-Yan Zhong, Ming Huang, Jian-Jian Chen, Jin-Ze Li, Hong-Tao Hu, Chang Zhao, Hai-Bin Shi, Zheng-Gang Ren, Hai-Bo Shao, Wei-Zhu Yang, Yang Zhao, Zhi-Cheng Jin, Xue-Feng Kan, Hai-Dong Zhu, Gao-Jun Teng","doi":"10.3350/cmh.2026.0693","DOIUrl":"https://doi.org/10.3350/cmh.2026.0693","url":null,"abstract":"<p><strong>Background: </strong>The treatment strategy for hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT) remains controversial because of its the dismal prognosis. This study aimed to evaluate the safety and efficacy of immune checkpoint inhibitors (ICIs) plus molecular-targeted agents (MTA) with or without hepatic arterial infusion chemotherapy (HAIC) as a first-line treatment for HCC with PVTT.</p><p><strong>Methods: </strong>This nationwide retrospective cohort study utilized a target trial emulation framework with a clone-censor-weighting (CCW) approach and was conducted in 36 centers across China. The study population comprised patients diagnosed with HCC and PVTT who received HAIC in combination with ICIs and MTA (HAIC-ICIs-MTA) or ICIs plus MTA (ICIs-MTA) from June 2018 to December 2024. The primary endpoint was overall survival (OS), which was evaluated through restricted mean survival time (RMST) with bootstrapping. Secondary endpoints included progression-free survival (PFS), objective response rate (ORR), and safety profiles.</p><p><strong>Results: </strong>This study included a total of 1649 HCC patients (614 in the HAIC-ICIs-MTA group and 1035 in the ICIs-MTA group). After CCW, the median OS of the HAIC-ICIs-MTA group was 23.3 months, whereas that of the ICIs-MTA group was 16.4 months. The difference in RMST for OS was 7.4 months (95% confidence interval [CI]: 3.5-11.7, bootstrapped P<0.001). The HAIC-ICIs-MTA group also had a significantly longer median PFS (8.7 months vs. 6.2 months, bootstrapped P=0.002) with an RMST of 2.6 months (95% CI: 0.9-4.5), and a higher ORR (38.9% vs. 22.7%, P<0.001) as per the Response Evaluation Criteria in Solid Tumors Version 1.1. Grade ≥3 treatment-related adverse events occurred in 243 patients in the HAIC-ICIs-MTA group (39.6%) and 335 patients in the ICIs-MTA group (32.4%).</p><p><strong>Conclusions: </strong>HAIC in combination with ICIs and MTA is associated with improved survival and an acceptable safety profile compared to ICIs plus MTA alone, supporting this regimen as a promising treatment strategy for HCC patients with PVTT that warrants further prospective validation.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic and Epitranscriptomic Regulation of Immune Checkpoint Response in Hepatocellular Carcinoma: Mechanisms, Therapeutic Targeting, and Translational Challenges.","authors":"Yafei Zhi, Yan Guo, Huifang Wei, Michael P Gantier, Xiwen Ma, Zigang Dong, Kangdong Liu","doi":"10.3350/cmh.2026.0745","DOIUrl":"https://doi.org/10.3350/cmh.2026.0745","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have reshaped systemic therapy for hepatocellular carcinoma (HCC), but durable benefit remains limited to a subset of patients because of tumor-intrinsic and microenvironmental mechanisms of immune resistance. Canonical epigenetic and epitranscriptomic alterations, including DNA methylation, histone modifications and chromatin remodeling, and epitranscriptomic RNA modifications, can influence tumor immune visibility by regulating antigen presentation, interferon responses, chemokine production, T-cell recruitment and function, and immunosuppressive programs in myeloid and stromal cells. This review critically evaluates HCC-specific evidence linking these regulatory mechanisms to immune checkpoint responsiveness. Emphasis is placed on crosstalk among DNA methylation, histone/chromatin regulation, and N6-methyladenosine (m6A)-dependent pathways; transcriptional-epigenetic stabilization of T-cell dysfunction; and epigenetic or epitranscriptomic remodeling of myeloid and stromal compartments, including cancer-associated fibroblasts. We further evaluate candidate therapeutic targets using a tiered evidence framework that integrates molecular association, mechanistic validation, pharmacologic validation, evidence from ICI-combination studies, and clinical validation. We assess therapeutic targets by evidence maturity and discuss emerging combination strategies and HCC-specific translational challenges, including chronic liver disease, limited hepatic reserve, and biomarker-guided patient selection. Although preclinical studies support several candidate mechanisms for modulating ICI responsiveness, mature clinical evidence for epigenetic-ICI combinations in HCC remains limited. These strategies should therefore be regarded as mechanistically compelling but clinically unproven and require rigorously designed, biomarker-integrated HCC trials with pharmacodynamic confirmation of immune reprogramming and careful safety evaluation.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TLR7 agonist plus anti-PD-L1 enhances HBsAg decline and reinvigorates HBV-specific CD8+ T cells: OCEANcure05 RCT study.","authors":"Yuying Chen, Ting Wu, Da Huang, Zhize Yuan, Ruiqi Zhai, Bingyao He, Wenyu Wu, Wei Yuan, Peng Wang, Zhongnan Xu, Shuna Wang, Dandan Huo, Meifang Han, Weiming Yan, Di Wu, Qin Ning","doi":"10.3350/cmh.2026.0476","DOIUrl":"https://doi.org/10.3350/cmh.2026.0476","url":null,"abstract":"<p><strong>Background & aims: </strong>TQ-A3334, a selective Toll-like receptor 7 (TLR7) agonist, activates innate immunity against hepatitis B virus (HBV). TQ-B2450, a humanized programmed death ligand 1 (PD-L1) antibody, could restore T cell function. This study assessed the safety, efficacy, and immunological profile of nucleos(t)ide analogues (NAs) plus TQ-A3334 with or without TQ-B2450 in virally suppressed patients with chronic hepatitis B (CHB).</p><p><strong>Methods: </strong>In the OCEANcure05 study (NCT04202653), 24 NAs-experienced patients with hepatitis B surface antigen (HBsAg) 250-5000 IU/mL were randomized to NAs monotherapy, dual therapy (NAs + TQ-A3334), or triple therapy (NAs + TQ-A3334 + TQ-B2450) for 24 weeks. The primary endpoint was HBsAg reduction at end of treatment (EOT). Single-cell RNA-seq and flow cytometry were conducted to characterize HBV-specific CD8+ T cell responses.</p><p><strong>Results: </strong>Triple therapy demonstrated numerically greater HBsAg reduction at EOT than dual therapy or monotherapy. Parallel trends were observed for HBV RNA and hepatitis B e antigen levels. In the triple therapy arm, baseline PD-L1 expression declined more markedly in patients with HBsAg decline ≥0.5 log10 IU/mL. Triple therapy increased IFN-γ, TNF-α, and CD107a expression in HBV-specific CD8+ T cells and broadened HBV peptide recognition. Reversible thyroid abnormalities were the predominant adverse event during triple therapy. No serious adverse events or deaths occurred.</p><p><strong>Conclusions: </strong>The combination therapy showed acceptable tolerability. In virally suppressed patients, the addition of PD-L1 antibody to NAs plus TLR7 agonist induced moderate HBsAg decline and elicited HBV-specific CD8+ T cell responses, supporting multi-target immunotherapy as a potential treatment strategy for CHB.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of Steatotic Liver Disease Subtypes based on the MetALD-ALD Prediction Index in the United States.","authors":"Donghee Kim, Pojsakorn Danpanichkul, Karn Wijarnpreecha, Aijaz Ahmed","doi":"10.3350/cmh.2026.0954","DOIUrl":"https://doi.org/10.3350/cmh.2026.0954","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward AI Virtual Cells for Hepatology: Representation, Generation, Dynamics, and Intervention in Single-Cell Models.","authors":"Youngseok Choi, In Gyeong Koh, Murim Choi, Joon-Yong An","doi":"10.3350/cmh.2026.0820","DOIUrl":"https://doi.org/10.3350/cmh.2026.0820","url":null,"abstract":"<p><p>``Single-cell and spatial atlases describe the healthy and diseased liver at high resolution, including lobular hepatocyte zonation, fibrotic macrophage-stellate niches, cholangiocyte reactions, immune remodeling, and hepatocellular carcinoma ecosystems. These maps show where cell states occur but do not, by themselves, predict whether liver injury will progress or how the liver will respond to an untested drug, toxicant, or genetic perturbation. In this review, we organize current approaches toward an AI Virtual Cell (AIVC) for the liver into three complementary modeling routes. Generative models represent cell states, dynamics and transport models infer state transitions, and pretrained or foundation models test whether learned representations transfer across donors, etiologies, disease stages, and platforms. Perturbation-response prediction serves as a cross-cutting assessment of whether these layers can predict responses to untested genetic, chemical, inflammatory, or metabolic interventions. Available evidence can be categorized as direct liver validation, liver-included benchmarks, general single-cell evidence, and conceptual applications. Published models demonstrate individual components, including atlas integration, inferred trajectories, transferable representations, and retrospective response programs. However, these models do not constitute a prospectively validated liver simulator. At minimum, evaluation should include donor-, etiology-, stage-, platform-, and perturbation-level hold-outs. Model performance should be reported using response direction, recovery of differentially expressed genes and rare states, and calibrated uncertainty. Claims about tissue- or function-level prediction additionally require independent spatial, histologic, metabolic, and functional readouts. Near-term use should prioritize experiment selection and hypothesis generation, whereas clinical decision support remains a longer-term objective.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148981960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNAi-mediated HBV antigen shutdown enhances the antiviral immune effects of PEGIFNα via T and B cell crosstalk remodeling.","authors":"Wenjing Zai, Kongying Hu, Mengying He, Ziyang Song, Pan Gao, Chen Luo, Minxiang Xie, Asha Ashuo, Min Yang, Jieliang Chen, Zhenghong Yuan","doi":"10.3350/cmh.2026.0385","DOIUrl":"https://doi.org/10.3350/cmh.2026.0385","url":null,"abstract":"<p><strong>Backgrounds/aims: </strong>PEGylated interferon-α (PEGIFNα) shows promise in treating chronic hepatitis B (CHB), yet patient response remains suboptimal. While suppressing hepatitis B virus (HBV) antigens by RNA interference (RNAi) could enhance PEGIFNα efficacy in CHB patients, the underlying immunological mechanisms remain obscure.</p><p><strong>Methods: </strong>Using our newly established extracellular humanized IFNAR (IFNAR-hEC) mouse model of chronic HBV infection, we evaluated the efficacy of a GalNac-conjugated siRNA (GalNac-siHBV) alone or in combination with PEGIFNα. Phenotypic and functional characteristics of immune cells were assessed by flow cytometry, ELISpot, and single-cell RNA sequencing (scRNA-seq).</p><p><strong>Results: </strong>High circulating HBsAg reduced antiviral effects and immune responsiveness of PEGIFNα. Combined PEGIFNα and RNAi therapy synergistically and durably suppressed HBsAg (~4log10 IU/mL, vs PBS) and achieved HBsAg seroconversion in ~30% of mice, outperforming either monotherapy. Mechanistically, PEGIFNα enhanced global T and B cell function, whereas combined therapy further amplified HBV-specific T and B cell responses. scRNA-seq analysis indicated that combined therapy attenuated inhibitory B cell-B cell interactions, strengthened MHC-I-mediated T cell crosstalk, and enhanced MHC-II signaling networks across B cells and hepatocytes/Cd8+ T cells, collectively improving the lymphocyte functionality and facilitating HBsAg seroconversion. Reinforcing MHC-I/II signaling with agonistic antibodies (α4-1BB, αCD40) or IL-2-Fc further potentiated antiviral immune responses of combinational regimen.</p><p><strong>Conclusions: </strong>Combined RNAi and PEGIFNα therapy exerts synergistic antiviral effects by relieving HBV antigen-induced immune tolerance and orchestrating a functional T cell-B cell crosstalk network centered on MHC-I/II signaling. Enhancing antigen presentation pathways represents a promising adjunctive strategy to improve functional cure rate of CHB.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocyte Plasticity in Liver Health and Disease: Zonation, Regeneration, Lineage Conversion, and Hepatic Malignancy.","authors":"Xuan Wang, Yunfang Wang, Shuyong Wang","doi":"10.3350/cmh.2026.0630","DOIUrl":"https://doi.org/10.3350/cmh.2026.0630","url":null,"abstract":"<p><p>Hepatocytes are highly specialized epithelial cells that maintain liver metabolic homeostasis, yet they also display remarkable plasticity in response to physiological demands, injury, disease, and oncogenic stress. In this review, we propose hepatocyte plasticity as an integrative framework that links homeostatic metabolic zonation, injury‑ and disease‑induced zonal remodeling and regeneration, hepatobiliary lineage conversion, and zonally biased malignant transformation. We first delineate homeostatic liver zonation as the baseline spatial architecture that constrains, rather than itself constitutes, hepatocyte plasticity, whereas dynamic re-zonation and state conversion represent plastic responses to perturbation. We further propose a conceptual framework that categorizes these plastic responses into four distinct yet interconnected modalities: transient adaptive state transitions, partial lineage conversion, transdifferentiation, and malignant lineage switching. We delineate the multiscale regulatory mechanisms underpinning each category, and critically assess the translational gaps between murine models and human disease. We further explore the therapeutic duality of this plasticity, evaluating emerging approaches that seek either to exploit its regenerative potential for liver repair and disease regression, or to counteract its pathological roles in cancer progression. By integrating these insights, this review establishes a comprehensive framework for understanding hepatocyte plasticity as a central determinant of liver pathobiology and highlights its translational potential for precision therapeutics in liver disease and cancer.</p>","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":" ","pages":""},"PeriodicalIF":21.7,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steatotic liver disease spectrum: From MASLD to MetALD and beyond - Clinical outcomes and precision medicine frontiers.","authors":"Won Kim","doi":"10.3350/cmh.2026.1072","DOIUrl":"10.3350/cmh.2026.1072","url":null,"abstract":"","PeriodicalId":10275,"journal":{"name":"Clinical and Molecular Hepatology","volume":"32 Suppl","pages":"e2026.1072"},"PeriodicalIF":21.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}