{"title":"New evidence of cross-disease communication between heart and liver","authors":"Thomas Marjot","doi":"10.1016/j.jhep.2024.11.034","DOIUrl":null,"url":null,"abstract":"","PeriodicalId":15888,"journal":{"name":"Journal of Hepatology","volume":"82 3","pages":"Pages 541-543"},"PeriodicalIF":26.8000,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Hepatology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0168827824027363","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
背景和背景关于代谢功能障碍相关脂肪性肝炎(MASH)的心血管影响,我们已经知道很多。心血管疾病(CVD)是MASH患者死亡的主要原因,尽管两种情况的危险因素重叠,但肝脂肪变性和炎症的存在通常被认为是缺血性心脏病(IHD)的独立危险因素。目的、方法和结果本研究主要涉及对有和没有MASH的啮齿动物进行急性心肌梗死(通过结扎左冠状动脉前降支)或假手术。然后,作者描述了肝脏表型、肝细胞浸润和对干预的全身免疫反应,然后使用一系列治疗条件,为心肌梗死后肝损伤的细胞和可溶性介质提供机制见解。首先,在三种具有科学重要性和翻译相关性的不同模型中发现心肌梗死会加剧肝损伤。在心肌梗死被认为是我们对人类MASH理解的重大转变之后,加速肝损伤的概念仍有一段路要走。目前工作的机制部分完全是在临床前模型中进行的,现在需要进一步的研究作为临床研究的一部分,尤其是因为啮齿动物和人类之间的脂质代谢和心血管结构都不同。此外,在财政支持t.m.后14天对肝脏病理进行单一评估。由国家卫生研究所(NIHR)学术临床讲师支持。所表达的观点是作者的观点,不一定是国家卫生服务(NHS)、国家卫生研究院或卫生部的观点。利益冲突。没有利益冲突要申报。详情请参阅随附的ICMJE披露表格。感谢Paul N Brennan博士(英国邓迪大学)对文章初稿的非正式审核。
期刊介绍:
The Journal of Hepatology is the official publication of the European Association for the Study of the Liver (EASL). It is dedicated to presenting clinical and basic research in the field of hepatology through original papers, reviews, case reports, and letters to the Editor. The Journal is published in English and may consider supplements that pass an editorial review.