JOURNAL OF HEPATOLOGY肝病学杂志
JOURNAL OF HEPATOLOGY(英文缩写 J HEPATOL),ISSN 0168-8278,eISSN 1600-0641,中文译名:肝病学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 30.083 | Q1 |
| 2022 | 25.700 | Q1 |
| 2023 | 26.800 | Q1 |
| 2024 | 33.000 | Q1 |
| 2025 | 40.100 | Q1 |
JOURNAL OF HEPATOLOGY 最新收录文献
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1. SETDB1: an epigenetic gatekeeper of antitumor immune organization in HCC.
1. SETDB1：肝细胞癌抗肿瘤免疫组织形成的表观遗传守门人PMID:日期:2026-10-03该文献暂无摘要。
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2. Authors' Reply to: "Beyond portal pressure: what does CIRI really predict?" and "Can the CIRI model reliably predict cACLD decompensation for clinical adoption?"
2. 作者对“超越门静脉压力：CIRI究竟能预测什么？”和“CIRI模型能否可靠预测cACLD失代偿以供临床采用？”的回复PMID:日期:2026-10-01该文献暂无摘要。
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3. Survival outcomes after liver transplantation in acute-on-chronic liver failure: A prospective study.
PMID:日期:2026-09-30The impact of liver transplantation (LT) on mortality among patients with advanced cirrhosis who have two organ failures (acute-on-chronic liver failure-2 [ACLF-2]) or ≥ three organ failures (ACLF-3) is unclear. Adults with decompensated cirrhosis with or without ACLF (grades 1-3), undergoing LT at 63 liver transplant centers worldwide were prospectively enrolled between 2021 and 2023 and followed for one year. Patients with ACLF-2 or ACLF-3 who were declined for LT were also prospectively followed for one year. Among the 144 patients declined for LT, 73% of those included with ACLF-2 and 88% of those with ACLF-3 died within 1 year. Of the 612 transplanted patients, 2% were re-transplanted and 12% died during the year. According to ACLF status at LT, the case-fatality rate without re-transplantation was 21% with ACLF-3 (42% when patients had five or six organ failures), 10.5% with ACLF-2, 10% with ACLF-1 (one organ failure), and 9% without ACLF. During the post-LT period, ACLF-3 patients experienced longer intensive care stay but similar ward stay, readmission rate and requirement for long-term renal replacement therapy. In time-to-event multivariable analyses, variables that were associated with higher post-LT mortality were being transplanted in Asia (vs. Europe or North America) or having ACLF-3 at LT (vs. no ACLF). The risk of dying after LT was similar in Asia vs. Latin America or with ACLF-2 vs. no ACLF. Patients with severe ACLF who underwent LT showed markedly better survival outcomes than those who were declined. Patients with five or six organ failures had high risk of post-LT death cautioning against routine LT in this population. ClinicalTrials.gov number, NCT04613921.
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4. Multi-target blood test for hepatocellular carcinoma early detection: a cross-sectional analysis of the prospective ALTUS study.
4. 用于肝细胞癌早期检测的多靶点血液检测：前瞻性ALTUS研究的横断面分析PMID:日期:2026-09-26Globally, 350 million people are at risk for HCC. Ultrasound screening is recommended but is limited by poor early-stage sensitivity and low adherence. This study evaluated whether the multi-target HCC blood test (mt-HBT) demonstrates non-inferior sensitivity for early-stage HCC compared with ultrasound and assessed its specificity. This prospective, multicenter study, conducted between July 2021 and June 2025 in the United States, evaluated the performance of the mt-HBT in a head-to-head comparison with standard-of-care ultrasound among adults with cirrhosis or chronic HBV infection who were eligible for routine HCC screening. All participants underwent computed tomography or magnetic resonance imaging as a reference standard. The co-primary outcomes were non-inferiority of mt-HBT to ultrasound for early-stage HCC sensitivity, with sequential testing of superiority, and mt-HBT specificity. A secondary outcome was overall (any-stage) mt-HBT sensitivity. Of 3089 participants, 2293 were evaluable with paired ultrasound and mt-HBT results. Thirty-seven HCCs were identified, with 27 classified as early stage by Milan criteria. Early-stage HCC sensitivities were 66.7% (95% CI, 47.8-81.4%) for mt-HBT and 22.2% (95% CI, 10.6-40.8%) for ultrasound, confirming mt-HBT non-inferiority within the prespecified 5% margin. The specificity for mt-HBT was 81.8% (95% CI, 80.1-83.4%), which did not meet the pre-specified co-primary outcome of 82%. Ultrasound specificity was 98.6% (95% CI, 98.0-99.0%). Any-stage HCC sensitivity was 73.0% (95% CI, 57.0-84.6%) for mt-HBT and 29.7% (95% CI, 17.5-45.8%) for ultrasound. No serious adverse events occurred during the blood collection process. The mt-HBT had higher observed sensitivity than ultrasound for early-stage HCC, with a paired absolute difference of 44.4% (95% CI, 20.2-63.8); however, specificity did not meet the prespecified target. The trial is registered with ClinicalTrials.gov (NCT05064553) IMPACT AND IMPLICATIONS: HCC screening remains limited by the suboptimal sensitivity of ultrasound, particularly among patients with obesity and steatotic liver disease. In this prospective multicenter study, a multi-target HCC blood test demonstrated substantially higher sensitivity for early-stage HCC detection than ultrasound while maintaining favorable screening performance across diverse patient subgroups. These findings are important for clinicians, researchers, and patients because they support further evaluation of blood-based approaches to address known limitations of imaging-based screening.
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5. Overall and Line-Specific Impact of Targeted Therapies in Advanced Biliary Tract Cancer After Chemoimmunotherapy Failure.
PMID:日期:2026-09-26The effectiveness and optimal timing of matched targeted therapy after first-line chemoimmunotherapy in biliary tract cancer (BTC) remain uncertain. We evaluated access to matched agents and line-specific outcomes. This retrospective study included 1,358 patients with advanced BTC treated with first-line cisplatin, gemcitabine, and durvalumab at 55 centers in 12 countries. Actionable alterations were defined as ESCAT tier I. The principal post-progression analysis excluded patients receiving best supportive care only and compared matched targeted therapy with active non-targeted treatment. Outcomes were assessed using Cox models, multivariable adjustment, inverse probability of treatment weighting, and landmark analyses. Molecular testing was performed in 1,072 patients and identified actionable alterations in 238 (22.2%); 76/238 (32.0%) received matched therapy. Among 125 patients receiving active treatment after first-line progression, matched therapy was associated with longer overall survival (OS) than non-targeted treatment (median 24.8 vs 16.6 months; HR 0.36, 95% CI 0.20-0.63; p=0.0004) and remained independently associated with improved OS (adjusted HR 0.35, 95% CI 0.22-0.56; p<0.0001). In the second-line cohort (n=127), matched therapy improved OS (HR 0.50, 95% CI 0.30-0.84; p=0.0009), progression-free survival (5.9 vs 3.2 months; HR 0.60, 95% CI 0.38-0.95; p=0.028), and objective response rate (27.1% vs 9.1%; p=0.010). No significant benefit was demonstrated in third line. Matched targeted therapy was associated with improved outcomes after chemoimmunotherapy failure, particularly when delivered in second line. Early molecular profiling and access to matched agents may reduce missed treatment opportunities. This study was undertaken to address a clinically relevant gap: whether the benefit of targeted therapies in molecularly selected advanced biliary tract cancer is maintained in real-world practice after chemoimmunotherapy failure, and whether timing of administration matters. The findings are important for clinicians, multidisciplinary teams, and patients because they show that matched targeted therapies were associated with longer survival, particularly when delivered in second line, while fewer than half of eligible patients ultimately received them in routine care. These results support early and systematic molecular profiling, ideally before first-line progression, to improve the likelihood that patients can access matched therapy while still fit for treatment. Given the retrospective design and the limited size of some molecular subgroups, these findings should be viewed as practice-informing and hypothesis-generating, while also highlighting the need for prospective validation and health-system strategies to improve access to precision oncology.
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6. Reply to: "From definitions to phenotyping: a response to the illusion of harmonisation".
6. 回复：“从定义到表型分析：对协调幻象的回应”PMID:日期:2026-09-26该文献暂无摘要。
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7. EBV-reactive KIR+ CX3CR1+ CD8+ T cells mediate liver transplantation tolerance.
7. EBV反应性KIR+ CX3CR1+ CD8+ T细胞介导肝移植耐受PMID:日期:2026-09-23Immune tolerance after transplantation reduces immunosuppression-related complications and improves the overall survival rates. The unique tolerogenic microenvironment of the liver enables a proportion of liver transplantation (LT) recipients to develop tolerance with intact liver function. However, the underlying immunological mechanisms remain unclear. s: We integrated single-cell transcriptome/TCR profiling, flow cytometry, in vitro killing assays, HLA-E peptidome from a retrospective cohort including 347 LT recipients, murine LT models, and a 20-participant prospective immunosuppressant withdrawal trial in pediatric LT recipients with median 26 months follow-up. We demonstrated that Epstein-Barr virus (EBV)-derived peptides can be presented by HLA-E on alloreactive CD4 T cells to prime KIR CX3CR1 CD8 T cells, thereby promoting immune tolerance after LT. As a subset of CD8 T cells, KIR CX3CR1 CD8 T cells utilize perforin and granzyme B to suppress alloreactive CD4 T cells after LT. In vitro analysis unveiled that the EBV-derived peptide SQAPLPCVL could stabilize HLA-E expression on alloreactive CD4 T cells and mediate recognition and elimination by KIR CX3CR1 CD8 T cells through a TCR-dependent mechanism. Furthermore, BATF was indispensable for induction of KIR CX3CR1 CD8 T cells. In the prospective immunosuppressant withdrawal clinical trial, the peripheral ratio of CD8 T and KIR CX3CR1 CD8 T cells were suggested to be potentially useful in identifying tolerant recipients. Our study demonstrated a new immune tolerance mechanism mediated by KIR CX3CR1 CD8 T cells and established the connection between viral infection and tolerance formation, providing new insights into tolerance-inductive strategies after transplantation.
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8. Precision support requires modifiable targets and inclusive reach in STOP-C.
8. 精准支持需要STOP-C中可修改的目标和包容性的覆盖范围PMID:日期:2026-09-23该文献暂无摘要。
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9. Restoration of aged liver regeneration by youthful systemic factors via LTβ-driven hepatocyte reprogramming.
9. 年轻全身性因子通过LTβ驱动的肝细胞重编程恢复衰老肝脏再生能力PMID:日期:2026-09-22The regenerative capacity of the liver decreases with age, limiting surgical options for elderly patients. While youthful systemic factors can reverse liver aging, the underlying mediators remain unclear. This study aimed to investigate the systemic factors and cellular mechanisms that promote aged liver regeneration. We retrospectively analyzed a split liver transplantation (SLT) cohort (n=36 pairs) to evaluate human graft regeneration. In animal models, 18-month-old and 2-month-old mice were subjected to heterochronic parabiosis, a procedure in which two animals of different ages were surgically connected to share a common circulation, followed by 70% partial hepatectomy. Single-cell transcriptomic profiling and lineage tracing were used to map hepatocyte dynamics. To elucidate the underlying mechanisms, hepatocyte-specific lymphotoxin β receptor (Ltbr) knockout and in vivo B-cell manipulations were employed to validate the key effectors and downstream signaling. In the SLT cohort, grafts in young recipients exhibited a significantly higher liver regeneration ratio than those in aged recipients. In murine experiments, heterochronic parabiosis significantly accelerated regeneration in aged mice. Single-cell transcriptomic profiling and lineage-tracing analyses revealed that aged periportal hepatocytes underwent transient somatic reprogramming to aid hepatocyte repopulation. Mechanistically, we discovered that this reprogramming was driven by young parabiont-derived lymphotoxin β (LTβ)/LTBR signaling. Further analysis identified young B cells as critical effectors, as these cells exhibited increased liver infiltration and elevated LTβ expression to promote hepatocyte reprogramming. Moreover, agonistic LTBR antibody administration successfully induced periportal reprogramming and accelerated aged liver regeneration. Young B-cell-derived LTβ promotes aged liver regeneration by promoting the transient somatic reprogramming of periportal hepatocytes via LTβ/LTBR signaling. Our study highlights the therapeutic potential of LTβ-based strategies to increase regeneration in aging populations. The regenerative capacity of the liver decreases with age, limiting the utilization of elderly grafts. This study demonstrates that youthful systemic circulation rejuvenates aged liver regeneration through young B-cell-derived lymphotoxin β (LTβ), which induces the transient somatic reprogramming of periportal hepatocytes via LTβ/LTBR signaling. These findings are highly relevant to transplant surgeons, hepatologists, and aging researchers. Practically, short-term pharmacological LTBR agonism could be utilized by clinicians to therapeutically "pre-condition" elderly donor livers or enhance post-hepatectomy regeneration in older patients. Furthermore, our work establishes heterochronic transplantation as a powerful clinical research platform to investigate anti-aging mechanisms and rejuvenation strategies across solid organs.