Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jun 21;178:114114. doi: 10.1016/j.bcp.2020.114114

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 Elsevier Inc. All rights reserved.

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

PMC Copyright notice

Fig. 1 — Relationship between ACE2 and SARS-CoV-2-related cardiovascular injury. (A) Organ distribution of ACE2 may be associated with clinical symptoms of COVID-19 patients. (B) Potential mechanism of cardiovascular injury induced by ACE2-mediated SARS-CoV-2 infection. SARS-CoV-2 uses ACE2 receptor for viral entry and replication. ACE2, but not ACE, is downregulated through binding of the spike protein of SARS-CoV-2 and ACE2. This leads to an increased level of Ang II and subsequent cardiovascular injury. (C) Impact of RAAS Blockers (ACEI and ARB) on cardiovascular system of COVID-19 patients. On the one hand, RAAS blockers upregulate the expression of ACE2, thereby leading to increased viral entry and replication and cardiovascular injury. On the other hand, RAAS blockers contribute to Ang II inhibition directly or indirectly (caused by upregulated ACE2), which may attenuate cardiovascular injury. AT1R, Ang II type 1 receptor; MasR, mitochondrial assembly receptor.