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Cardiovasc Res. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2

tetano

Editor, Senior Moderator
Cardiovasc Res. 2020 Mar 30. pii: cvaa078. doi: 10.1093/cvr/cvaa078. [Epub ahead of print]
The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2.


Chen L[SUP]1[/SUP], Li X[SUP]2[/SUP], Chen M[SUP]3[/SUP], Feng Y[SUP]4[/SUP], Xiong C[SUP]1[/SUP].

Author information




Abstract

A new type of pneumonia caused by a novel coronavirus SARS-CoV-2 outbreaks recently in China and spreads into many other countries. This disease, named as COVID-19, is similar to patients infected by SARS-CoV and MERS-CoV, and nearly 20% of patients developed severe condition. Cardiac injury is a prevalent complication of severe patients, exacerbating the disease severity in coronavirus disease 2019 (COVID-19) patients. Angiotensin-converting enzyme 2 (ACE2), the key host cellular receptor of SARS-CoV-2, has been identified in multiple organs, but its cellular distribution in human heart is not illuminated clearly. This study performed the first state-of-art single cell atlas of adult human heart, and revealed that pericytes with high expression of ACE2 might act as the target cardiac cell of SARS-CoV-2. The pericytes injury due to virus infection may result in capillary endothelial cells dysfunction, inducing microvascular dysfunction. And patients with basic heart failure disease showed increased ACE2 expression at both mRNA and protein levels, meaning that if infected by the virus these patients may have higher risk of heart attack and critically ill condition. The finding of this study explains the high rate of severe cases among COVID-19 patients with basic cardiovascular disease; and these results also perhaps provide important reference to clinical treatment of cardiac injury among severe patients infected by SARS-CoV-2.
Published on behalf of the European Society of Cardiology. All rights reserved. ? The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.



KEYWORDS:

ACE2; Heart failure; Heart injury; SARS-CoV-2


PMID:32227090DOI:10.1093/cvr/cvaa078
 
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