Journal of Clinical and Translational Hepatology最新文献

{"title":"Serum miR-381-3p: Diagnostic Role and Mechanisms in Liver Transplant Ischemia-reperfusion Injury.","authors":"Xiaobin Chi, Zerun Lin, Zhijian Chen, Jianda Yu, Yongbiao Chen, Honghuan Lin, Qiucheng Cai, Lizhi Lv","doi":"10.14218/JCTH.2025.00571","DOIUrl":"10.14218/JCTH.2025.00571","url":null,"abstract":"<p><strong>Background and aims: </strong>Hepatic ischemia-reperfusion (HIR) injury impairs outcomes post-liver transplantation. Therefore, we aimed to investigate the role and mechanism of miR-381-3p in HIR.</p><p><strong>Methods: </strong>The study enrolled 150 healthy controls, 82 non-HIR-injured patients, and 68 patients with HIR injury following liver transplantation. Clinical data were analyzed. Multivariate analysis identified HIR risk factors; the predictive value of miR-381-3p was assessed via receiver operating characteristic analysis. An <i>in vitro</i> hypoxia/reoxygenation (H/R) model was established and employed. The cellular effects of miR-381-3p and JAK2 were evaluated using CCK-8, flow cytometry, ELISA, luciferase, RIP, and bioinformatics.</p><p><strong>Results: </strong>Serum miR-381-3p was significantly elevated in HIR compared with the other groups. miR-381-3p was the strongest independent HIR risk factor, which was confirmed by receiver operating characteristic analysis. H/R upregulated miR-381-3p. Inhibiting miR-381-3p counteracted H/R-induced decreased viability and increased apoptosis, inflammation, and oxidative stress. miR-381-3p directly bound to and suppressed JAK2 via its 3' untranslated region (validated by luciferase and RIP). Transfection of si-JAK2 abolished the protective effects of miR-381-3p inhibition.</p><p><strong>Conclusions: </strong>miR-381-3p exacerbates post-transplant HIR by directly targeting JAK2, amplifying inflammation and oxidative stress. Thus, our findings nominate serum miR-381-3p as a promising non-invasive biomarker and suggest its potential as a therapeutic target for mitigating HIR injury.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"177-186"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433087","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":"Prognostic Nutritional Index Predicts Outcomes in Hepatocellular Carcinoma Treated with Atezolizumab and Bevacizumab: A Propensity Score-matched Analysis.","authors":"Yuan-Hung Kuo, Wei Teng, Yen-Hao Chen, Po-Ting Lin, Tsung-Han Wu, Chung-Wei Su, Wei-Ting Chen, Chen-Chun Lin, Chao-Hung Hung, Sheng-Nan Lu, Shi-Ming Lin, Jing-Houng Wang, Chun-Yen Lin","doi":"10.14218/JCTH.2025.00418","DOIUrl":"10.14218/JCTH.2025.00418","url":null,"abstract":"<p><strong>Background and aims: </strong>The prognostic nutritional index (PNI), calculated from serum albumin and lymphocyte count, reflects a patient's immune-nutritional status and has been proposed as a prognostic marker in hepatocellular carcinoma (HCC). However, its role in advanced HCC patients treated with atezolizumab plus bevacizumab (Ate/Bev) remains unclear. In this study, we aimed to evaluate the prognostic value of PNI in patients receiving first-line Ate/Bev therapy.</p><p><strong>Methods: </strong>We retrospectively analyzed 362 patients with unresectable HCC who received Ate/Bev between November 2020 and June 2023 across two centers. Based on prior literature, a cutoff of 45 was used to classify patients into low-PNI (<45) and high-PNI (≥45) groups. Propensity score matching was performed to balance baseline characteristics.</p><p><strong>Results: </strong>After propensity score matching, 130 patients (65 per group) were included in the analysis. The high-PNI group showed a significantly lower incidence of grade ≥ 3 treatment-related adverse events (10.8% vs. 24.6%, <i>p</i> = 0.039), a higher objective response rate (38.4% vs. 20.0%, <i>p</i> = 0.037), and significantly longer overall survival (16.7 vs. 7.9 months, <i>p</i> = 0.009). Although progression-free survival was longer in the high-PNI group (4.8 vs. 3.0 months), the difference was not statistically significant (<i>p</i> = 0.597). Multivariate analysis confirmed that PNI was an independent predictor of overall survival (hazard ratio: 0.574, 95% confidence interval: 0.353-0.933, <i>p</i> = 0.025), after adjusting for vascular invasion, alpha-fetoprotein levels, concurrent therapy, and post-treatment interventions.</p><p><strong>Conclusions: </strong>PNI is an independent prognostic factor for overall survival in advanced HCC patients treated with Ate/Bev in real-world clinical practice. Incorporating PNI into routine assessments may enhance risk stratification and guide therapeutic decision-making.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"168-176"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433045","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":"Eight-year Results from Two Randomized Phase 3 Trials of Tenofovir Alafenamide for Chronic Hepatitis B Virus Infection in China.","authors":"Jinlin Hou, Qin Ning, Zhongping Duan, Yu Chen, Qing Xie, Lunli Zhang, Shanming Wu, Hong Tang, Jun Li, Feng Lin, Yongfeng Yang, Guozhong Gong, Yanwen Luo, Yan Chen, Frida Abramov, Leland J Yee, Hongyuan Wang, Roberto Mateo, Tahmineh Yazdi, Irina Botros, Chengwei Chen, Yan Huang, Mingxiang Zhang, Jidong Jia","doi":"10.14218/JCTH.2025.00438","DOIUrl":"10.14218/JCTH.2025.00438","url":null,"abstract":"<p><strong>Background and aims: </strong>Tenofovir alafenamide (TAF) has demonstrated comparable efficacy to tenofovir disoproxil fumarate (TDF), with improved renal and bone safety, in Chinese participants with chronic hepatitis B enrolled in two Phase 3 trials. This study aimed to evaluate the long-term virologic efficacy, serological and biochemical responses, resistance, and renal and bone safety of TAF over eight years in this population.</p><p><strong>Methods: </strong>Participants completing the three-year double-blind phase were eligible to receive open-label TAF 25 mg/day for up to an additional five years (totaling eight years). Analyses of viral suppression (HBV DNA < 29 IU/mL), alanine aminotransferase normalization, serological responses, resistance surveillance, and safety outcomes were conducted.</p><p><strong>Results: </strong>Among 334 enrolled participants, 212 of 227 participants randomized to TAF continued open-label TAF (TAF-TAF), and 99 of 107 participants on TDF switched to open-label TAF (TDF-TAF). At Year 8, 79.3% (180/227) and 78.5% (84/107) of participants in the TAF-TAF and TDF-TAF groups, respectively, achieved viral suppression (missing = failure); rates increased to 95.2% (180/189) and 95.5% (84/88) when excluding missing data. Alanine aminotransferase normalization rates remained high and comparable between groups. Serologic response rates continued to increase over time, with higher rates observed in the TAF-TAF group. Estimated glomerular filtration rate (by Cockcroft-Gault) and hip/spine bone mineral density remained stable in the TAF-TAF group through eight years; the small declines in these renal and bone parameters observed during double-blind TDF treatment improved after switching to open-label TAF. No resistance to TAF was detected.</p><p><strong>Conclusions: </strong>Long-term TAF treatment demonstrated durable virologic efficacy, sustained biochemical and serological responses, and favorable renal and bone safety over eight years in Chinese participants with chronic hepatitis B.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"146-158"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433110","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":"Metabolic Risk Factors and Clinical Presentations of Metabolic Dysfunction-associated Steatotic Liver Disease Using Data from the <i>All of Us</i> Research Program.","authors":"Ke-Qin Hu, Seyedeh Neelufar Payrovnaziri, Argyrios Ziogas, Steven Hiek, Kuangda Shan, Tevan Luong, Jenny Fang, Hoda Anton-Culver","doi":"10.14218/JCTH.2025.00393","DOIUrl":"10.14218/JCTH.2025.00393","url":null,"abstract":"<p><strong>Background and aims: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 32% of the US adult population. The present study aimed to utilize the All of Us electronic health record-linked large cohort to assess seven metabolic risk factors (MRFs) simultaneously, the impact by ethnicity and age, and clinical presentations of MASLD.</p><p><strong>Methods: </strong>This study included a MASLD group (n = 15,060) and a frequency-matched control group (n = 75,300). Multivariable analyses were performed to compare the frequencies of MRFs and clinical outcomes between the two groups. Type 1 diabetes was not included in the multivariable analysis. Subgroup analyses were conducted according to race and ethnicity, as well as age.</p><p><strong>Results: </strong>The overall frequency of MASLD was 6.0%. Compared with the control group, individuals with MASLD had significantly higher independent frequencies of obesity (66.1% vs. 41.3%), type 2 diabetes (39.5% vs. 16.9%), hypertension (64.3% vs. 38.6%), hyperlipidemia (59.8% vs. 37.3%), obstructive sleep apnea (28.9% vs. 13.4%), and hypothyroidism (21.2% vs. 13.4%). Obesity was identified as the strongest independent MRF among Asians, Whites, and Hispanics, particularly in individuals younger than 50 years, whereas hypertension was the strongest independent MRF in Blacks. MASLD was also associated with significantly higher frequencies of cardiac events, including coronary artery disease (17.1% vs. 9.4%) and myocardial infarction (7.1% vs. 4.2%); hepatic events, including cirrhosis (7.5% vs. 1.1%) and hepatocellular carcinoma (0.5% vs. 0.1%); and elevated liver enzymes, including alanine aminotransferase (27.7% vs. 10.1%), aspartate aminotransferase (18.0% vs. 6.4%), and alkaline phosphatase (19.8% vs. 13.1%), compared with the control group.</p><p><strong>Conclusions: </strong>Our study demonstrated that obesity, hypertension, hyperlipidemia, type 2 diabetes, obstructive sleep apnea, and hypothyroidism were independent MRFs for MASLD overall, but the ranking of these MRFs by odds ratios could vary by ethnicity and age. MASLD presents with significantly higher rates of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase elevation, as well as cardiac and hepatic events.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"137-145"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433120","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":"Cathepsin K Alleviates Liver Fibrosis by Inhibiting the TGF-β/Smad Signaling Pathway and Inducing Hepatic Stellate Cell Apoptosis.","authors":"Zhandong Lin, Yue Shi, Mengjiao Sun, Jiawei Cui, Dandan Zhao, Yaoyao Mao, Congyue Zhang, Ying Zhang, Qianqian Zheng, Yukai Chen, Shaoya Li, Yuemin Nan","doi":"10.14218/JCTH.2025.00592","DOIUrl":"10.14218/JCTH.2025.00592","url":null,"abstract":"<p><strong>Background and aims: </strong>Liver fibrosis is characterized by the excessive deposition of extracellular matrix, a process primarily driven by activated hepatic stellate cells (HSCs), and currently lacks effective therapy. Cathepsin K (CTSK) exhibits context-dependent roles across organ systems in fibrosis, but its function in liver fibrosis is unclear. This study aimed to investigate the role and underlying mechanisms of CTSK during liver fibrosis.</p><p><strong>Methods: </strong>CTSK expression was analyzed in human fibrotic liver samples via transcriptomic analysis and confirmed in murine fibrosis models. The function of CTSK was investigated in both primary HSCs and LX-2 cells by assessing its effects on cell activation, proliferation, apoptosis, and the underlying signaling pathways following CTSK overexpression. The therapeutic potential was evaluated using an adeno-associated virus serotype 8 to overexpress CTSK in two etiologically distinct murine fibrosis models.</p><p><strong>Results: </strong>CTSK was upregulated in activated HSCs and fibrotic livers. Furthermore, we discovered that it mediates a negative feedback loop to inhibit the TGF-β/Smad pathway via Smad7/Smurf2-dependent TGF-β receptor-I degradation, thereby suppressing HSC activation and proliferation. CTSK also induced mitochondrial apoptosis through Bax/Bcl-2 imbalance and caspase-3 activation. Together, these actions contribute to the anti-fibrotic effect of CTSK. Notably, adeno-associated virus serotype 8-mediated CTSK overexpression attenuated liver fibrosis across multiple murine models.</p><p><strong>Conclusions: </strong>Our study demonstrates that elevated CTSK functions as an endogenous protective factor that attenuates liver fibrosis. CTSK mediates negative feedback inhibition of the TGF-β pathway while concurrently promoting the mitochondrial apoptosis pathway. The dual anti-fibrotic mechanisms identify CTSK as a promising therapeutic target for liver fibrosis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"187-201"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12968025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433076","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":"Traditional and Novel Virologic Markers for Functional Cure and HBeAg Loss with Pegylated Interferon in Chronic Hepatitis B: A Systematic Review and Meta-analysis.","authors":"Ying Zhang, Long-Fei Wang, Jing Chen, Mindie H Nguyen, Qi Zheng","doi":"10.14218/JCTH.2025.00443","DOIUrl":"10.14218/JCTH.2025.00443","url":null,"abstract":"<p><strong>Background and aims: </strong>The rate of functional cure (HBsAg loss) remains unsatisfactory following pegylated interferon (PEG-IFN) treatment in chronic hepatitis B. To optimize PEG-IFN administration, this study aimed to evaluate virological markers to predict functional cure and/or hepatitis B e antigen (HBeAg) loss.</p><p><strong>Methods: </strong>Relevant studies assessing virologic markers for predicting functional cure and HBeAg loss after PEG-IFN therapy were systematically retrieved from PubMed, Embase, the Cochrane Library, and Web of Science up to November 2023. Predictive effectiveness was evaluated via the summary receiver operating characteristic curve.</p><p><strong>Results: </strong>We analyzed 38 studies (6,179 patients). HBsAg decline at week 24 had the greatest discriminative ability according to the area under the receiver operating characteristic curve (AUROC) (0.89) and sensitivity (0.88) for predicting functional cure, whereas baseline HBsAg had a comparable AUROC (0.86) and highest specificity (0.79), with both being significantly better than baseline hepatitis B core-related antigen and hepatitis B virus (HBV) RNA (all <i>P</i> < 0.001). For HBeAg loss or seroconversion, HBV RNA, HBV DNA, HBeAg, and HBeAg decline at week 12, as well as HBV DNA and HBeAg decline at week 24, all exhibited comparable predictive values (AUROC = 0.75-0.78). HBV RNA and HBeAg levels at week 24 showed optimal sensitivity (0.87), and HBeAg decline at week 12 had the highest specificity (0.83).</p><p><strong>Conclusions: </strong>HBsAg decline at week 24 and baseline HBsAg levels are better predictors of functional cure than novel virologic markers, while on-treatment HBV RNA and HBeAg levels and dynamic changes are the most reliable indicators for HBeAg loss.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"159-167"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433040","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":"Tumor Vaccines in Hepatocellular Carcinoma: Advances, Challenges, and the Path Toward Precision Immunotherapy.","authors":"Bin Niu, Jun Xu, Liaoyun Zhang","doi":"10.14218/JCTH.2025.00401","DOIUrl":"10.14218/JCTH.2025.00401","url":null,"abstract":"<p><p>Primary hepatocellular carcinoma (HCC) remains one of the leading causes of cancer-related mortality worldwide, with curative options still limited for patients with advanced disease. As an emerging modality of cancer immunotherapy, tumor vaccines represent a promising approach that activates the host immune system to recognize and eliminate malignant cells. Multiple vaccine platforms, including peptide vaccines, dendritic-cell vaccines, nucleic-acid vaccines, and viral-vector vaccines, have been explored for HCC. Among these, peptide- and dendritic-cell-based vaccines are supported by the most extensive clinical data, demonstrating favorable safety and immunogenicity profiles. The advent of personalized therapeutic cancer vaccines based on tumor-specific antigens has further refined the precision of vaccine design. Nevertheless, several major challenges persist, including immune suppression within the tumor immune microenvironment, marked tumor heterogeneity, immune-escape mechanisms, and limited vaccine immunogenicity, all of which hinder clinical efficacy. In addition, issues related to standardization, large-scale production, and regulatory oversight remain unresolved. Recent advances in sequencing technology, nanotechnology, and artificial intelligence have opened new avenues for optimizing vaccine platforms and delivery strategies. Combination therapies that integrate cancer vaccines with immune checkpoint inhibitors, chemotherapy, or locoregional treatments are also being actively investigated to improve patient outcomes. In summary, although vaccine-based immunotherapy for HCC is still at an early stage, its integration with personalized medicine and multimodal therapeutic strategies holds great potential for improving the long-term prognosis of patients with HCC. Therefore, this review aims to systematically summarize current advances in tumor vaccine-based immunotherapy for hepatocellular carcinoma, with a particular focus on vaccine platforms, target antigens, clinical trial outcomes, and future challenges for clinical translation.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"202-214"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433085","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":"Immune Checkpoint Inhibitor-induced Liver Injury: A Critical Appraisal of Treatment and Rechallenge Controversies.","authors":"Fernando Bessone, Nelia Hernandez","doi":"10.14218/JCTH.2025.00450","DOIUrl":"10.14218/JCTH.2025.00450","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"240-244"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433047","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":"Repurposing SGLT2 Inhibitors for Cirrhotic Ascites: From Mechanistic Research to Clinical Exploration.","authors":"Yuan Gao, Yunyi Gao, Dong Ji, Zhongjie Hu","doi":"10.14218/JCTH.2025.00465","DOIUrl":"10.14218/JCTH.2025.00465","url":null,"abstract":"<p><p>Cirrhotic ascites develops when portal hypertension and arterial under-filling chronically activate neuro-hormonal pathways that drive renal sodium-water retention. Augmented proximal tubular sodium reabsorption, predominantly mediated by the apical sodium/hydrogen exchanger 3 (NHE3), plays a fundamental role in this process. Given the spatial coupling of NHE3 and the sodium-glucose cotransporter 2 (SGLT2), selective SGLT2 inhibition reduces NHE3 activity via functional suppression within the apical microdomain. The increased sodium chloride delivery to the macula densa augments tubuloglomerular feedback and modulates the renin-angiotensin-aldosterone system. Early clinical investigations, ranging from case reports and retrospective analyses to pilot randomized trials, indicated potential benefits in controlling ascites and reducing decompensation events. However, their limited sample size, heterogeneous endpoints, and predominantly observational design constrain the generalizability of the findings. This review concentrates on the molecular mechanisms and emerging clinical evidence supporting the therapeutic potential of SGLT2 inhibitors in the management of cirrhotic ascites.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 2","pages":"232-239"},"PeriodicalIF":6.0,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433064","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":"Expert Consensus on the Diagnosis and Management of Inherited Hyperbilirubinemia (2025).","authors":"Sujun Zheng, Xiaoyuan Xu, Yuemin Nan, Wei Hou, Jie Bai, Shan Tang, Chen Liang, Lei Luo, Jianshe Wang, Xinhua Li, Min Zhang, Guohong Deng, Hui Liu, Yongfeng Yang, Wen Xie, Xiaojuan Ou, Xinxin Zhang, Lai Wei, Jidong Jia, Zhongping Duan","doi":"10.14218/JCTH.2025.00440","DOIUrl":"10.14218/JCTH.2025.00440","url":null,"abstract":"<p><p>To support clinicians in making informed decisions regarding the diagnosis and management of inherited hyperbilirubinemia, including Gilbert syndrome, Crigler-Najjar syndrome, Dubin-Johnson syndrome, and Rotor syndrome, the Inherited and Metabolic Liver Disease Collaboration Group of the Hepatology Branch of the Chinese Medical Association convened a panel of Chinese experts in this field. This multidisciplinary consortium developed the present expert consensus by integrating the latest advances in both clinical practice and basic research.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"14 1","pages":"83-95"},"PeriodicalIF":4.2,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12872385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142504","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}