Angiotensin II Receptors ‐ Impact for COVID‐19 Severity

Aksoy, H; Karadag, AS; Wollina, U

COVID‐19 is an outbreak of viral pneumonia which became a global health crisis, and the risk of morbidity and mortality of people with obesity are higher. SARS‐CoV‐2, the pathogen of COVID‐19, enters into cells through binding to the Angiotensin Converting Enzyme (ACE) homolog‐2 (ACE2). ACE2 is a regulator of two contrary pathways in renin angiotensin system (RAS): ACE‐Ang‐II‐AT1R axis and ACE2‐Ang 1‐7‐Mas axis. Viral entry process eventuate in downregulation of ACE2 and subsequent activation of ACE‐Ang‐II‐AT1R axis. ACE‐Ang II‐AT1R axis increases lipid storage, reduces white‐to‐beige fat conversion and plays role in obesity. Conversely, adipose tissue is an important source of angiotensin, and obesity results in increased systemic RAS. ACE‐Ang‐II‐AT1R axis, which has proinflammatory, profibrotic, prothrombotic and vasoconstrictive effects, is potential mechanism of more severe SARS‐CoV‐2 infection. The link between obesity and severe COVID‐19 may be attributed to ACE2 consumption and subsequent ACE‐Ang‐II‐AT1R axis activation. Therefore, patients with SARS‐CoV‐2 infection may benefit from therapeutic strategies that activate ACE2‐Ang 1‐7‐Mas axis, such as Ang II reseptor blockers (ARBs), ACE inhibitors (ACEIs), Mas receptor agonists and ACE2. This article is protected by copyright. All rights reserved.