The discovery that SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) RNA 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.
The authors declare that there was no funding for this work.
- Mone Zaidi, Icahn School of Medicine at Mount Sinai, United States
- 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)
© 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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