Journal of Clinical and Translational Hepatology最新文献

{"title":"Lipid Metabolism-related lncRNA Model Identifies <i>AC026412.3</i> as a Driver of Fatty Acid β-oxidation in Hepatocellular Carcinoma.","authors":"Lixin Liu, Yuhao Fan, Hao Zou, Sheng Hu, Kui Long, Lianghua Li, Chaosheng Xia, Hongyue Wang, Yang Liu, Runlin Feng, Zongqi Deng, Qiang Kang","doi":"10.14218/JCTH.2026.00312","DOIUrl":"10.14218/JCTH.2026.00312","url":null,"abstract":"<p><strong>Background and aims: </strong>Dysregulated lipid metabolism contributes to hepatocellular carcinoma (HCC) progression, but the prognostic value and mechanistic roles of lipid metabolism-related long noncoding RNAs (LRLs) remain insufficiently characterized. This study aimed to construct and validate an LRL-based prognostic model and to investigate the biological function and metabolic mechanism of <i>AC026412.3</i> in HCC.</p><p><strong>Methods: </strong>Transcriptomic and clinical data from the The Cancer Genome Atlas Liver Hepatocellular Carcinoma cohort were analyzed to identify LRLs based on their correlation with curated lipid metabolism genes. Differential expression, univariate Cox, least absolute shrinkage and selection operator (LASSO), and multivariate Cox analyses were performed to construct a prognostic signature, which was evaluated using Kaplan-Meier survival and time-dependent receiver operating characteristic (ROC) analyses. Functional enrichment analyses Gene Ontology [GO], Kyoto Encyclopedia of Genes and Genomes [KEGG] and gene set enrichment analysis [GSEA], mutation profiling, tumor mutational burden, immune infiltration estimation, and consensus clustering were applied to characterize associated features. A key LRL was identified through integrated bioinformatic screening and prioritization. Its biological role was assessed by quantitative reverse transcription polymerase chain reactionq (RT-PCR), western blotting, BODIPY staining, colony formation, Transwell assays, and xenograft models. RNA sequencing followed by pathway enrichment analysis was conducted to explore underlying mechanisms.</p><p><strong>Results: </strong>A three-LRL signature (<i>AL031985.3</i>, <i>NRAV</i>, and <i>AC026412.3</i>) stratified HCC patients into distinct risk groups with significantly different survival outcomes and demonstrated independent prognostic value. <i>AC026412.3</i> was markedly upregulated in HCC and associated with poor prognosis. Functional assays demonstrated that <i>AC026412.3</i> promoted proliferation, invasion, and tumor growth while reducing lipid accumulation. Mechanistically, <i>AC026412.3</i> upregulated solute carrier family 22 member 5 (SLC22A5), enhanced fatty acid β-oxidation, and increased adenosine triphosphate (ATP) production, thereby driving metabolic reprogramming.</p><p><strong>Conclusions: </strong>This study establishes a robust LRL-based prognostic model and identifies <i>AC026412.3</i> as a key regulator of lipid metabolic reprogramming via the SLC22A5-fatty acid β-oxidation axis, highlighting its potential as a biomarker and therapeutic target in HCC.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"842-856"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Efficacy of Promising Targets in the Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Steatohepatitis: A Systematic Review and Network Meta-analysis.","authors":"Wenjing Ni, Jie Li, Xue Bai, Sisi Zhou, Xiangyu Wu, Leyao Jia, Zhuoru Jiang, Jiali Wu, Ming Li, Connie Wong, Chao Wu, Junping Shi, Mindie H Nguyen","doi":"10.14218/JCTH.2025.00596","DOIUrl":"10.14218/JCTH.2025.00596","url":null,"abstract":"<p><strong>Background and aims: </strong>Randomized controlled trials (RCTs) have been conducted to evaluate treatment efficacy for metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis. This study aimed to compare the effectiveness and safety of 11 promising targets among adults with MASLD.</p><p><strong>Methods: </strong>PubMed, Web of Science, the Cochrane Central Register of Controlled Trials, Scopus, and Embase were searched from inception to November 20, 2024. The primary outcomes were fibrosis improvement ≥1 stage without worsening of steatohepatitis and steatohepatitis resolution without worsening of fibrosis. Additional outcomes included reductions in liver fat content, liver enzymes, metabolic profiles, and selected safety outcomes. The surface under the cumulative ranking curve (SUCRA) was used to rank efficacy.</p><p><strong>Results: </strong>Of 11,584 articles screened, 44 eligible RCTs (11,410 participants, 33 medications) were included. For fibrosis improvement, d-(R)-pioglitazone (SUCRA: 79.3) and fibroblast growth factor (FGF) 21 analogs (SUCRA: 71.9) ranked higher. For steatohepatitis resolution, glucagon-like peptide-1 (GLP-1)/glucose-dependent insulinotropic polypeptide (GIP) dual receptor agonists (RAs) (SUCRA: 91.7) ranked higher. Co-agonists of GLP-1/GIP/GCG and GLP-1/GCG receptors ranked higher for relative and absolute changes in liver fat content, respectively. For liver enzymes and glucose improvement, the combination of a GLP-1 RA and an acetyl-coenzyme A carboxylase inhibitor ranked higher. GLP-1 RAs, peroxisome proliferator-activated RAs, and FGF21 analogs showed favorable effects on lipid profile improvement.</p><p><strong>Conclusions: </strong>Incretin-based co-agonists and FGF21 analogs showed favorable profiles across key endpoints, while d-(R)-pioglitazone and GLP-1/GIP dual RAs ranked higher for fibrosis improvement and steatohepatitis resolution, respectively. SUCRA rankings should be interpreted in conjunction with effect sizes, uncertainty, and available safety data.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"810-823"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Berberine Attenuates Hepatic Sinusoidal Obstruction Syndrome by Inhibiting Endothelial-mediated Neutrophil Recruitment and Activation.","authors":"Yiken Lin, Wenjia Tian, Weiming Dai, Ning Chen, Huifeng Hao, Yulan Liu","doi":"10.14218/JCTH.2026.00024","DOIUrl":"10.14218/JCTH.2026.00024","url":null,"abstract":"<p><strong>Background and aims: </strong>Hepatic sinusoidal obstruction syndrome (HSOS) is a life-threatening liver vascular disorder with limited treatment options. HSOS results from the activation and injury of liver sinusoidal endothelial cells (LSECs). Berberine (BBR) has been shown to protect endothelial cells in various diseases. However, whether BBR can alleviate liver injury and LSEC disruption in HSOS remains unclear. In this study, we aimed to evaluate the effect of BBR on HSOS.</p><p><strong>Methods: </strong>Two mouse models of HSOS were established using monocrotaline or oxaliplatin. Mice in the treatment groups received a low dose (100 mg/kg) or a high dose (200 mg/kg) of BBR daily. Histology, scanning electron microscopy, immunofluorescence, and flow cytometry were used to evaluate the therapeutic effects of BBR. Cell co-culture, Transwell assays, qRT-PCR, and Western blotting were performed to investigate the molecular pathways involved.</p><p><strong>Results: </strong>BBR treatment dose-dependently reduced liver injury and disruption of LSECs in murine HSOS models. Moreover, BBR significantly reduced hepatic neutrophil infiltration, thereby attenuating neutrophil-mediated injury to LSECs. Additionally, BBR inhibited the effect of injured LSECs on neutrophil activation. Mechanistically, injured LSECs were identified as one of the major sources of CXCL1 in HSOS, and BBR downregulated CXCL1 expression in injured LSECs by inhibiting MAPK signaling.</p><p><strong>Conclusions: </strong>In this study, we demonstrate that BBR ameliorates HSOS by inhibiting endothelial-mediated neutrophil recruitment and activation. BBR may be a promising therapeutic option for HSOS treatment.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"799-809"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Basis and Clinical Significance of the High-risk Phenotype of Hepatitis B Virus Genotype C.","authors":"Chenchen Huang, Zhongjian Liu, Jingyao Zhang, Tao Shen, Lei Sang","doi":"10.14218/JCTH.2026.00247","DOIUrl":"10.14218/JCTH.2026.00247","url":null,"abstract":"<p><p>Hepatitis B virus (HBV) genotype C is common in East Asia and is associated with poor outcomes, particularly liver cirrhosis and hepatocellular carcinoma (HCC). Clinically, genotype C infection has been associated with persistent viral replication, delayed HBeAg seroconversion, more active hepatic inflammation, and an increased risk of HCC. Current evidence suggests that these features are driven by several key molecular events, including the A1762T/G1764A double mutation in the basal core promoter, the G1896A mutation in the precore region, abnormal hepatitis B virus X protein function, and viral integration. Together, these changes may reshape viral transcription, antigen expression, host immune interactions, and oncogenic signaling, thereby contributing to disease progression and hepatocarcinogenesis. Other factors, such as epigenetic changes, dysregulated DNA damage responses, impaired tumor protein p53 function, and disrupted autophagy, may also be involved, although their exact roles remain unclear. Notably, even after effective viral suppression with potent nucleos(t)ide analogs, patients with genotype C may still have a relatively high residual risk of HCC. This review summarizes the molecular virological features, pathogenic mechanisms, immune dysregulation, and clinical significance of HBV genotype C, and discusses the potential value of genotype information in risk stratification, long-term surveillance, and clinical assessment of chronic hepatitis B.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"865-878"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"qHBsAg Trajectories with Peg-IFNα-2b Add-on Therapy in Nucleos(t)ide Analog-experienced HBeAg-positive Chronic Hepatitis B.","authors":"Kezhen Hu, Yanzhen Bi, Xiaoying Li, Xiangzhong Liu, Haoxi Wang, Yong Zhou, Yongning Xin","doi":"10.14218/JCTH.2026.00175","DOIUrl":"10.14218/JCTH.2026.00175","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"879-882"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma Metabolites for Identifying Bacterial Infection in Acute-on-chronic Liver Failure: A Prospective Multicenter Study.","authors":"Xiaotian Yang, Hai Li, Yan Huang, Guohong Deng, Beiling Li, Xianbo Wang, Zhongji Meng, Yubao Zheng, Yanhang Gao, Zhiping Qian, Feng Liu, Xiaobo Lu, Yu Shi, Jia Shang, Jing Liu, Hang Jia, Sumeng Li, Lining Guo, Xin Zheng","doi":"10.14218/JCTH.2026.00384","DOIUrl":"10.14218/JCTH.2026.00384","url":null,"abstract":"<p><strong>Background and aims: </strong>Bacterial infection is a key cause of mortality in patients with acute-on-chronic liver failure (ACLF). In this study, we aimed to identify metabolite biomarkers and develop a novel machine learning model for early identification of bacterial infection in ACLF.</p><p><strong>Methods: </strong>Based on a prospective multicenter cohort from 14 centers, 1,314 patients with acute-on-chronic liver disease were enrolled, including those with ACLF and non-ACLF. Plasma samples at admission were collected for metabolomics profiling. Patients were randomly divided into discovery (n = 921) and validation (n = 393) sets. Machine learning was used to develop diagnostic models. The win ratio method was employed to assess the risk stratification capability of the models.</p><p><strong>Results: </strong>Bacterial infection occurred in 198 of the 451 ACLF patients and 132 of the 863 non-ACLF patients. Infection altered the plasma metabolome, especially in lipid, amino acid, and xenobiotic metabolic pathways. Models for bacterial infection in ACLF (five metabolites) and non-ACLF (six metabolites) demonstrated superior discrimination in the discovery (AUCs: 0.881 and 0.935, respectively) and validation sets (AUCs: 0.835 and 0.889, respectively) compared with C-reactive protein, white blood cell count, procalcitonin, and the best composite clinical model. Metabolic risk stratification based on the models effectively predicted 90-day outcomes (all-cause death, organ failure, sepsis, new-onset acute decompensation, and systemic inflammatory response syndrome).</p><p><strong>Conclusions: </strong>Our models based on novel metabolic biomarkers enable identification of patients at high risk of bacterial infection and support risk stratification of 90-day outcomes.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"771-784"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of Peg-INF plus TDF versus TDF Monotherapy in Indeterminate-phase Chronic Hepatitis B Patients with High HBsAg levels, HBeAg-negative status, and Normal ALT Levels.","authors":"Min Liu, An Xiao, Bing Bu, Lili Zuo, Yuting Zhang, Ling Zhu, Liping Huang, Yilan Wang, Jinbo Luo, Wei Yue, Jiawei Geng","doi":"10.14218/JCTH.2026.00015","DOIUrl":"10.14218/JCTH.2026.00015","url":null,"abstract":"<p><strong>Background and aims: </strong>Chronic hepatitis B patients with baseline hepatitis B surface antigen (HBsAg) <1500 IU/mL are considered as the favorable population for achieving functional cure. This trial aimed to explore a treatment strategy to help the unfavorable population characterized by high HBsAg levels (>3000 IU/mL), hepatitis B e antigen-negative status, and normal alanine transaminase levels in the indeterminate phase (HBeIP), transition to the favorable group.</p><p><strong>Methods: </strong>In this investigator-initiated, open-label clinical trial, we randomly assigned participants aged 18 to 60 years with HBeIP characteristics to receive either tenofovir disoproxil fumarate (TDF) monotherapy (monotherapy group) or pegylated interferon alfa-2b (Peg-IFNα-2b) plus TDF (combination group). The primary endpoints were the HBsAg loss rate and the proportion of participants with HBsAg <1,500 IU/mL through week 96.</p><p><strong>Results: </strong>From May 2021 to November 2023, we enrolled 263 participants, with 131 randomly assigned to the combination group and 132 to the monotherapy group. In the primary analysis, none of the 132 participants (0%) in the monotherapy group achieved HBsAg loss, compared with 10 of 131 (7.6%) in the combination group (<i>P</i> = 0.001). Through week 96, 48.9% (64/131) of participants in the combination group achieved HBsAg <1,500 IU/mL, and a reduction in HBsAg level greater than 1 log₁₀ IU/mL between baseline and week 24 was an independent predictor of this endpoint (Odds Ratio = 16.957, 95% Confidence Interval: 3.002-95.797, <i>P</i> = 0.001). In contrast, only two participants (1.5%) in the monotherapy group achieved HBsAg <1,500 IU/mL.</p><p><strong>Conclusions: </strong>Compared with TDF monotherapy, combination therapy with Peg-IFNα-2b and TDF significantly improved both HBsAg <1,500 IU/mL and HBsAg loss rates in HBeIP patients.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"857-864"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Prediction of Non-recovery in Drug-induced Liver Injury by Integrating Genetic Variants and Clinical Variables: An Interpretable Machine Learning Approach.","authors":"Jingjing Jiang, Weiwei Lou, Qing Li, Ziqiang Li, Weiqian Lou, Xichen Zhu, Qing Xie, Rongtao Lai","doi":"10.14218/JCTH.2026.00447","DOIUrl":"10.14218/JCTH.2026.00447","url":null,"abstract":"<p><strong>Background and aims: </strong>Early predictors of 6-month non-recovery in drug-induced liver injury (DILI) remain limited. Genetic variants are stable host characteristics that may complement baseline clinical variables. We aimed to develop and validate an interpretable, clinical-genetic machine learning model for predicting 6-month non-recovery in patients with DILI.</p><p><strong>Methods: </strong>This retrospective, single-center study included 338 patients with DILI, who were classified as recovered (n = 171) or non-recovered (n = 167) at 6 months. Candidate single-nucleotide polymorphisms and baseline clinical variables were collected during initial hospitalization. Features were selected using complementary screening approaches. Multiple machine learning models were developed and compared. Model discrimination, calibration, clinical utility, the incremental value of genetic predictors, and interpretability using SHapley Additive exPlanations (SHAP) were assessed.</p><p><strong>Results: </strong>Five predictors were consistently retained for model development: rs72631567, rs28521457, alanine aminotransferase, monocyte percentage, and low-density lipoprotein. Among the candidate algorithms, the light gradient boosting machine model showed the best performance, with area under the receiver operating characteristic curve (AUC) values of 0.92 (95% confidence interval [CI] 0.89-0.95) in the training set and 0.81 (95% CI 0.70-0.91) in the validation set. The model showed acceptable calibration and favorable decision-curve performance. In ablation analysis, the clinical-only model showed limited discrimination (AUC 0.57, 95% CI 0.43-0.71). SHAP analysis identified rs72631567 as the most influential predictor.</p><p><strong>Conclusions: </strong>An interpretable model that integrates host genetic variants with baseline clinical variables demonstrated good internal performance for early prediction of 6-month non-recovery in DILI. These findings support external validation of genotype-informed risk stratification in patients with DILI.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 8","pages":"785-798"},"PeriodicalIF":6.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Lipid Metabolism Reprogramming in Hepatocellular Carcinoma.","authors":"Weiqi Duan, Qian Jian, Bo Sun, Hong Yang, Youcai Deng, Yu Peng, Sulai Liu","doi":"10.14218/JCTH.2026.00055","DOIUrl":"10.14218/JCTH.2026.00055","url":null,"abstract":"<p><p>Lipid metabolism reprogramming drives malignant proliferation and invasiveness in hepatocellular carcinoma (HCC). Beyond supplying energy and membrane components, lipids function as signaling molecules that modulate tumor cell epigenetics and the microenvironment. Accumulating research has clarified the implications of these metabolic alterations in HCC, providing a rationale for targeted therapies. This review summarizes key alterations in lipid metabolism within HCC and explores their mechanistic contributions to tumor progression. It further examines how lipid metabolic shifts in immune and stromal cells of the tumor microenvironment promote HCC advancement. Finally, we discuss the therapeutic potential of targeting lipid metabolism in liver cancer treatment.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 7","pages":"743-755"},"PeriodicalIF":6.0,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expanding the Horizon: A Roadmap for Artificial Intelligence Integration in Metabolic Dysfunction-associated Steatotic Liver Disease.","authors":"Abdulrahman Ismaiel, Stefan-Lucian Popa","doi":"10.14218/JCTH.2026.00266","DOIUrl":"10.14218/JCTH.2026.00266","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 7","pages":"768-769"},"PeriodicalIF":6.0,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}