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Postgrad Med J . ACE2 and COVID-19 and the Resulting ARDS

tetano

Editor, Senior Moderator
Postgrad Med J


. 2020 Jun 10;postgradmedj-2020-137935.
doi: 10.1136/postgradmedj-2020-137935. Online ahead of print.
ACE2 and COVID-19 and the Resulting ARDS


Xiaoqing Zhang[SUP] 1 2 [/SUP], Shuren Li[SUP] 3 [/SUP], Shaoqian Niu[SUP] 2 [/SUP]



Affiliations

Abstract

This article reviews the correlation between ACE2 and COVID-19 and the resulting acute respiratory distress syndrome (ARDS). ACE2 is a crucial component of the renin-angiotensin system (RAS). The classical ACE-angiotensin Ⅱ (Ang II)-angiotensin type 1 receptor (AT1R) axis and the ACE2-Ang(1-7)-Mas counter-regulatory axis play an essential role in RAS system. ACE2 antagonises the activation of the classical RAS ACE-Ang II-AT1R axis and protects against lung injury. Similar to severe acute respiratory syndrome-related coronavirus, 2019 novel coronavirus (2019-nCoV) also uses ACE2 for cell entry. ARDS is a clinical high-mortality disease which is probably due to the excessive activation of RAS caused by 2019-nCoV infection, and ACE2 has a protective effect on ARDS caused by COVID-19. Because of these protective effects of ACE2 on ARDS, the development of drugs enhancing ACE2 activity may become one of the most promising approaches for the treatment of COVID-19 in the near future. In the meantime, however, the use of RAS blockers such as ACE inhibitors and angiotensin II receptor blockers that inhibit the damaging (ACE-Ang II) arm of the RAS cascade in the lung may also be promising. Trial registration number: NCT04287686.
 
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