Renin-angiotensin system and SARS-CoV-2 interaction: underlying mechanisms and potential clinical implications.

Abstract

Renin-angiotensin system (RAS) inhibition supposedly increases the expression of angiotensin converting enzyme 2, serving as a binding site for SARS-CoV-2. Concerns arose regarding therapy with RAS inhibition during the COVID-19 pandemic. However, the pharmacological restraining the classical RAS axis might be beneficial due to the reduction of deleterious effects of angiotensin II and enhancement of the anti-inflammatory angiotensin 1-7 pathway. Unless large controlled studies are performed, RAS inhibition remains the cornerstone therapy in populations with cardiovascular disorders.

• Authors: Jaroslav Hrenak, Stefan Zorad, Fedor Simko
• Journal: General physiology and biophysics (Gen Physiol Biophys) Vol. 39 Issue 3 Pg. 203-204 (May 2020) ISSN: 0231-5882 [Print] Slovakia
• PMID: 32525813 (Publication Type: Letter)

Chemical References

• Angiotensin II Type 1 Receptor Blockers
• Angiotensin-Converting Enzyme Inhibitors
• Angiotensin II
• Peptidyl-Dipeptidase A
• ACE2 protein, human
• Angiotensin-Converting Enzyme 2

Topics

• Angiotensin II (blood)
• Angiotensin II Type 1 Receptor Blockers (therapeutic use)
• Angiotensin-Converting Enzyme 2
• Angiotensin-Converting Enzyme Inhibitors (therapeutic use)
• Betacoronavirus (pathogenicity, physiology)
• COVID-19
• Cardiovascular Diseases (complications, drug therapy)
• Coronavirus Infections (complications, drug therapy)
• Humans
• Pandemics
• Peptidyl-Dipeptidase A
• Pneumonia, Viral (complications, drug therapy)
• Renin-Angiotensin System
• SARS-CoV-2
• Virus Internalization (drug effects)