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SARS-CoV-2 诱导心肌细胞损伤的直接机制:最新进展。

Direct mechanisms of SARS-CoV-2-induced cardiomyocyte damage: an update.

机构信息

Center for Pulmonary Vascular Diseases, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases of China, State Key Laboratory of Cardiovascular, Beijing, 100037, China.

Center for Coronary Heart Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases of China, State Key Laboratory of Cardiovascular, Beijing, 100037, China.

出版信息

Virol J. 2022 Jun 25;19(1):108. doi: 10.1186/s12985-022-01833-y.

Abstract

Myocardial injury induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is reportedly related to disease severity and mortality, attracting attention to exploring relevant pathogenic mechanisms. Limited by insufficient evidence, myocardial injury caused by direct viral invasion of cardiomyocytes (CMs) is not fully understood. Based on recent studies, endosomal dependence can compensate for S protein priming to mediate SARS-CoV-2 infection of CMs, damage the contractile function of CMs, trigger electrical dysfunction, and tip the balance of the renin-angiotensin-aldosterone system to exert a myocardial injury effect. In this review, we shed light on the direct injury caused by SARS-CoV-2 to provide a comprehensive understanding of the cardiac manifestations of coronavirus disease 2019 (COVID-19).

摘要

据报道,严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的心肌损伤与疾病严重程度和死亡率有关,这引起了人们对探索相关发病机制的关注。由于证据不足,人们对病毒直接侵袭心肌细胞(CMs)引起的心肌损伤还不完全了解。基于最近的研究,内体依赖性可以弥补 S 蛋白的引发作用,从而介导 SARS-CoV-2 对 CMs 的感染,损害 CMs 的收缩功能,引发电功能障碍,并使肾素-血管紧张素-醛固酮系统失衡,发挥心肌损伤作用。在这篇综述中,我们探讨了 SARS-CoV-2 对心肌的直接损伤,以期全面了解 2019 冠状病毒病(COVID-19)的心脏表现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/669b/9233758/ee4942ee3068/12985_2022_1833_Fig1_HTML.jpg

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