The role of SARS-CoV-2 target ACE2 in cardiovascular diseases

Abstract

SARS-CoV-2, the virus responsible for the global coronavirus disease (COVID-19) pandemic, attacks multiple organs of the human body by binding to angiotensin-converting enzyme 2 (ACE2) to enter cells. More than 20 million people have already been infected by the virus. ACE2 is not only a functional receptor of COVID-19 but also an important endogenous antagonist of the renin-angiotensin system (RAS). A large number of studies have shown that ACE2 can reverse myocardial injury in various cardiovascular diseases (CVDs) as well as is exert anti-inflammatory, antioxidant, anti-apoptotic and anticardiomyocyte fibrosis effects by regulating transforming growth factor beta, mitogen-activated protein kinases, calcium ions in cells and other major pathways. The ACE2/angiotensin-(1-7)/Mas receptor axis plays a decisive role in the cardiovascular system to combat the negative effects of the ACE/angiotensin II/angiotensin II type 1 receptor axis. However, the underlying mechanism of ACE2 in cardiac protection remains unclear. Some approaches for enhancing ACE2 expression in CVDs have been suggested, which may provide targets for the development of novel clinical therapies. In this review, we aimed to identify and summarize the role of ACE2 in CVDs.

Keywords: ACE2; RAS; SARS-CoV-2; cardiovascular diseases.

FIGURE 1

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) binds to angiotensin‐converting enzyme 2 (ACE2) and induces ACE2 shedding to produce soluble ACE2 in serum, which triggers an angiotensin II (Ang II)‐mediated inflammation response

FIGURE 2

A diagram depicting the method for up‐regulating ACE2 expression and the downstream molecular mechanism of ACE2 in cardiovascular diseases (CVDs)