Hepatology最新文献_第5页

Accurate identification and risk-stratification of HBeAg-negative indeterminate phase of chronic hepatitis B: not all shades of grey are the same 慢性乙型肝炎hbeag阴性不确定期的准确识别和风险分层：并非所有灰色阴影都是相同的

IF 13.5 1区医学

Hepatology Pub Date : 2025-04-15 DOI: 10.1097/hep.0000000000001353

Tai-Chung Tseng, Anna Suk-Fong Lok

引用次数: 0

Reply: Primary sclerosing cholangitis and autoimmune hepatitis - distinct or common autoimmune penetrance? 回复：原发性硬化性胆管炎和自身免疫性肝炎——不同的还是共同的自身免疫性外显？

IF 13.5 1区医学

Hepatology Pub Date : 2025-04-11 DOI: 10.1097/hep.0000000000001326

Aiva Lundberg Båve,Erik von Seth,Michael Ingre,Caroline Nordenvall,Annika Bergquist

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Targeting the ER stress sensor IRE1 protects the liver from fibrosis through the downregulation of the proteostasis factor P4HB/PDIA1. IRE1以内质网应激传感器为靶点，通过下调蛋白酶抑制因子P4HB/PDIA1来保护肝脏免受纤维化。

IF 12.9 1区医学

Hepatology Pub Date : 2025-04-09 DOI: 10.1097/HEP.0000000000001335

Younis Hazari, Lama Habbouche, Valeria A Garcia Lopez, Hery Urra, Javier Diaz, Giovanni Tamburini, Mateus Milani, Sylvere Durand, Fanny Aprahamian, Reese Baxter, Menghao Huang, X Charlie Dong, Luis Gonzalez-Rojas, Juan Francisco Silva, Ignacio Tapia-Dufey, Helena Vihinen, Vlad Ratziu, Fabienne Foufelle, Jan G Hengstler, Eija Jokitalo, Jessica L Maiers, Lars Plate, Guido Kroemer, Beatrice Bailly-Maitre, Claudio Hetz

{"title":"Targeting the ER stress sensor IRE1 protects the liver from fibrosis through the downregulation of the proteostasis factor P4HB/PDIA1.","authors":"Younis Hazari, Lama Habbouche, Valeria A Garcia Lopez, Hery Urra, Javier Diaz, Giovanni Tamburini, Mateus Milani, Sylvere Durand, Fanny Aprahamian, Reese Baxter, Menghao Huang, X Charlie Dong, Luis Gonzalez-Rojas, Juan Francisco Silva, Ignacio Tapia-Dufey, Helena Vihinen, Vlad Ratziu, Fabienne Foufelle, Jan G Hengstler, Eija Jokitalo, Jessica L Maiers, Lars Plate, Guido Kroemer, Beatrice Bailly-Maitre, Claudio Hetz","doi":"10.1097/HEP.0000000000001335","DOIUrl":"https://doi.org/10.1097/HEP.0000000000001335","url":null,"abstract":"<p><p>Collagen is the main cargo of the secretory pathway, contributing to hepatic fibrogenesis due to extensive accumulation of extracellular matrix. An excess of collagen deposition is a characteristic feature of several chronic liver diseases. Collagen overproduction imposes pressure on the secretory pathway, altering endoplasmic reticulum (ER) proteostasis. Here we investigated the possible contribution of the unfolded protein response UPR, the main adaptive pathway that monitors and adjusts protein production capacity at the ER, to collagen biogenesis and liver disease. Genetic ablation of the ER stress sensor IRE1 in the liver using conditional knockout mice reduced liver damage and collagen deposition in models of fibrosis, steatosis, and acute hepatotoxicity. Proteomic profiling identified the prolyl 4-hydroxylase (P4HB, also known as PDIA1) as a major IRE1-regulated gene, a critical factor involved in collagen maturation. Cell culture studies demonstrated that IRE1 deficiency results in collagen retention at the ER, reducing its secretion, and this phenotype is rescued by P4HB/PDIA1 overexpression. Analyses of human MASH samples revealed a positive correlation between IRE1 signaling and P4HB/PDIA1 expression as well as the severity of the disease. Altogether, our results establish a role of the IRE1/P4HB axis in the regulation of collagen production and support its implication in the pathogenesis of liver fibrosis.</p>","PeriodicalId":177,"journal":{"name":"Hepatology","volume":" ","pages":""},"PeriodicalIF":12.9,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810137","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}

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Reply: Post-TIPS hemodynamic target adherence fails to improve outcomes in cirrhotic patients. 回答：tips后血液动力学靶标依从性不能改善肝硬化患者的预后。

IF 12.9 1区医学

Hepatology Pub Date : 2025-04-08 DOI: 10.1097/HEP.0000000000001350

Davide Roccarina, Dario Saltini, Marco Senzolo, Silvia Nardelli, Stefania Gioia, Lara Biribin, Fabio Marra, Filippo Schepis, Francesco Vizzutti

引用次数: 0

Reply: Considerations on the use of LPCN 1148 in cirrhotic patients with sarcopenia. 回复：关于在肝硬化肌肉减少患者中使用LPCN 1148的考虑。

IF 12.9 1区医学

Hepatology Pub Date : 2025-04-08 DOI: 10.1097/HEP.0000000000001348

Benjamin J Bruno, Joshua C Weavil, Jonathan Ogle, Nachiappan Chidambaram, Anthony DelConte, Mahesh V Patel, Elizabeth J Carey, Arun J Sanyal, Jennifer C Lai

引用次数: 0

Letter to the editor: Considerations on the use of LPCN 1148 in cirrhotic patients with sarcopenia. 致编辑：关于在肝硬化肌肉减少症患者中使用LPCN 1148的考虑。

IF 12.9 1区医学

Hepatology Pub Date : 2025-04-08 DOI: 10.1097/HEP.0000000000001347

Xinxing Tantai, Lu Li, Shejiao Dai

引用次数: 0

Letter to the editor: Post-TIPS hemodynamic target adherence fails to improve outcomes in cirrhotic patients. 致编辑的信：tips后的血液动力学目标依从性未能改善肝硬化患者的预后。

IF 12.9 1区医学

Hepatology Pub Date : 2025-04-08 DOI: 10.1097/HEP.0000000000001349

Xinxing Tantai, Lu Li, Shejiao Dai

引用次数: 0

Erratum: Mitogen-activated protein kinase kinase kinase 4 deficiency in intrahepatic cholangiocarcinoma leads to invasive growth and epithelial-mesenchymal transition 在肝内胆管癌中，有丝分裂原活化蛋白激酶激酶激酶4缺乏导致侵袭性生长和上皮-间质转化

IF 13.5 1区医学

Hepatology Pub Date : 2025-04-07 DOI: 10.1097/hep.0000000000001274

Liu-Xiao Yang, Qiang Gao, Jie-Yi Shi, Zhi-Chao Wang, Yong Zhang, Ping-Ting Gao, Xiao-Ying Wang, Ying-Hong Shi, Ai-Wu Ke, Guo-Ming Shi, Jia-Bin Cai, Wei-Ren Liu, Meng Duan, Ying-Jun Zhao, Yuan Ji, Dong-Mei Gao, Kai Zhu, Jian Zhou, Shuang-Jian Qiu, Ya Cao, Qi-Qun Tang, Jia Fan

引用次数: 0

Portal sinusoidal vascular diseases: Assessment and therapy 门窦血管疾病：评估与治疗

IF 13.5 1区医学

Hepatology Pub Date : 2025-04-07 DOI: 10.1097/hep.0000000000001344

Maria Mironova, Harish Gopalakrishna, Christopher Koh, David E. Kleiner, Theo Heller

{"title":"Portal sinusoidal vascular diseases: Assessment and therapy","authors":"Maria Mironova, Harish Gopalakrishna, Christopher Koh, David E. Kleiner, Theo Heller","doi":"10.1097/hep.0000000000001344","DOIUrl":"https://doi.org/10.1097/hep.0000000000001344","url":null,"abstract":"The term porto-sinusoidal vascular disease (PSVD) was introduced in 2019 to describe a group of liver conditions that can lead to portal hypertension (PH) in the absence of cirrhosis or portal vein thrombosis, with or without specific findings on liver histology. The new nomenclature has facilitated the consolidation of knowledge on diseases previously referred to by various terms, including Banti’s disease, non-cirrhotic portal hypertension, non-cirrhotic portal fibrosis, and idiopathic portal hypertension, while excluding certain etiologies like sarcoidosis, congenital hepatic fibrosis, and Budd-Chiari syndrome. The prevalence and recognition of the disorder has been increasing. Advances in diagnostics and treatment have improved life expectancy for patients with associated conditions, such as immunodeficiencies and autoimmune diseases. Similar to cirrhosis, patients with PSVD may experience complications of PH, including variceal bleeding and ascites. However, less is known about its natural history, screening strategies, prognosis, and treatment options. This review discusses methods for assessing PSVD, including clinical and histological features, imaging techniques, and currently available treatments. It also addresses the challenges posed by the new nomenclature and the remaining questions in disease assessment.","PeriodicalId":177,"journal":{"name":"Hepatology","volume":"60 1","pages":""},"PeriodicalIF":13.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143798359","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}

引用次数: 0

Simulating the impact of survival benefit-based liver transplant organ allocation 模拟基于生存福利的肝移植器官分配的影响

IF 13.5 1区医学

Hepatology Pub Date : 2025-04-07 DOI: 10.1097/hep.0000000000001338

David Goldberg, Catherine Blandon, Cindy Delgado, Binu John, Ezekiel Emanuel, David Kaplan, Peter Reese

{"title":"Simulating the impact of survival benefit-based liver transplant organ allocation","authors":"David Goldberg, Catherine Blandon, Cindy Delgado, Binu John, Ezekiel Emanuel, David Kaplan, Peter Reese","doi":"10.1097/hep.0000000000001338","DOIUrl":"https://doi.org/10.1097/hep.0000000000001338","url":null,"abstract":"Background & Aims: In the US, and much of the world, prioritization for a deceased donor liver transplant focuses on sickest-first based on allocating organs using the MELD score. There have been calls to instead allocate organs based on transplant survival benefit, but the impact of such a system on the broader waitlist population is unknown. Approach & Results: We performed a simulation study using the Liver Simulated Allocation Model (LSAM) to compare the current US system of liver allocation to one, using different time horizons, focused on: pre-transplant survival only, post-transplant survival only, and survival benefit (difference of post-transplant survival and pre-transplant survival). Changing liver allocation to a survival benefit-based system was simulated to lead to a small improvement in average patient-level post-transplant survival (mean survival over 5-year time horizon of 4.24 y vs. 4.19 y in current system). However, this small improvement was associated with a simulated decrease in transplants and an increase in waitlist mortality of 400 deaths per year. The resulting net benefit overall (pre-transplant deaths and post-transplant survival) was negligible under a survival benefit-based allocation approach. Conclusions: Our simulations predicted that survival benefit-based allocation would only increase post-transplant survival by an average of 18 days per recipient, at the expense of a simulated increase in waitlist mortality of 400 deaths per year. The current practice of liver transplantation, with sickest-first allocation operating in a system where transplant physicians ration organs to maximize outcomes, survival benefit overall is maintained and not compromised.","PeriodicalId":177,"journal":{"name":"Hepatology","volume":"13 1","pages":""},"PeriodicalIF":13.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797954","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}

引用次数: 0