Abstract
The discovery that SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) binds to the angiotensin converting enzyme (ACE)-2, which is highly expressed in the lower airways, explained why SARS-CoV-2 causes acute respiratory distress syndrome (ARDS) and respiratory failure. After this, news spread that ACEis and ARBs would be harmful in SARS-CoV-2-infected subjects. To the contrary, compelling evidence exists that the ACE-1/angiotensin(Ang)II/ATR-1 pathway is involved in SARS-CoV-2-induced ARDS, while the ACE-2/Ang(1-7)/ATR2/MasR pathway counteracts the harmful actions of AngII in the lung. A reduced ACE-1/ACE-2 ratio is, in fact, a feature of ARDS that can be rescued by human recombinant ACE-2 and Ang(1-7) administration, thus preventing SARS-CoV-2-induced damage to the lung. Based on the current clinical evidence treatment with ACE-inhibitors I (ACEis) or angiotensin receptor blockers (ARBs) continues to provide cardiovascular and renal protection in patients diagnosed with COVID-19. Discontinuing these medications may therefore be potentially harmful in this patient population.
Article and author information
Author details
Funding
The authors declare that there was no funding for this work.
Reviewing Editor
- Mone Zaidi, Icahn School of Medicine at Mount Sinai, United States
Publication history
- Received: March 26, 2020
- Accepted: April 3, 2020
- Accepted Manuscript published: April 6, 2020 (version 1)
- Accepted Manuscript updated: April 8, 2020 (version 2)
- Accepted Manuscript updated: April 9, 2020 (version 3)
- Accepted Manuscript updated: April 15, 2020 (version 4)
- Version of Record published: May 4, 2020 (version 5)
- Version of Record updated: May 6, 2020 (version 6)
Copyright
© 2020, Rossi et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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