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冠状病毒感染对心血管系统的损伤及可能机制

Damage of cardiovascular system by new coronavirus infection and its possible mechanism

  • 摘要: 冠状病毒(coronavirus,CoVs)感染主要累及肺部,但对心血管系统损伤作用也不容忽视。CoVs感染引起的心脏损伤并非罕见,其发生与病情的严重程度密切相关。本文首先从CoVs引起心血管损伤的证据入手,进一步探讨了CoVs对心肌的直接损伤,以及肾素血管紧张素(RAS)系统激活和细胞因子风暴与炎症反应对心血管损伤的可能作用机制。相关心血管损伤的可能机制包括,(1)病毒直接作用:CoVs在心肌细胞复制,损伤心肌;(2)RAS系统激活:感染CoVs后,心脏血管紧张素转化酶2(angiotensin-converting enzyme 2,ACE2)的表达下调,激活RAS系统,使得血管紧张素Ⅱ(Angiotensin Ⅱ,Ang Ⅱ)收缩血管功能增强,Ang1-7保护心脏效应减弱;(3)诱发细胞因子风暴:循环细胞因子和全身炎症反应引起心脏损伤;(4)其他:包括低氧血症和儿茶酚胺心脏毒性。本文就相关内容作一综述,为后续的详尽机制和治疗策略研究提供思路。

     

    Abstract: Coronavirus (coronavirus, CoVs) infection mainly affects the lungs. However, the effect of CoVs on cardiovascular system damage can not be ignored. Previous studies have shown that heart injury caused by CoVs infection is not rare, and its occurrence is closely related to the severity of the disease. Starting with the evidence of cardiovascular injury caused by CoVs, this paper further discusses the direct myocardial injury caused by CoVs, and the possible mechanism of RAS system activation, cytokine storm and inflammation on cardiovascular injury, and the possible mechanisms of cardiovascular injury, including:(1) direct action of virus:CoVs replicates in cardiomyocytes and injures myocardium; (2) activation of RAS system:after infection with CoVs, the expression of ACE2 is down-regulated and RAS system is activated, which enhances the vasoconstrictive function of Ang Ⅱ and weakens the protective effect of Ang1-7; (3) inducing cytokine storm:cardiac injury caused by circulating cytokines and systemic inflammatory response; (4) others:including hypoxemia and catecholamine cardiotoxicity. The purpose of this paper is to provide ideas for the follow-up detailed mechanism and treatment strategy research.

     

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