| Literature DB >> 33881142 |
Fedor Simko1,2,3, Tomas Baka1.
Abstract
Angiotensin-converting enzyme 2 (ACE2) is the leading player of the protective renin-angiotensin system (RAS) pathway but also the entry receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). RAS inhibitors seemed to interfere with the ACE2 receptor, and their safety was addressed in COVID-19 patients. Pedrosa et al. (Clin. Sci. (Lond.) (2021), 135, 465-481) showed in rats that captopril and candesartan up-regulated ACE2 expression and the protective RAS pathway in lung tissue. In culture of pneumocytes, the captopril/candesartan-induced ACE2 up-regulation was associated with inhibition of ADAM17 activity, counterbalancing increased ACE2 expression, which was associated with reduced SARS-CoV-2 spike protein entry. If confirmed in humans, these results could become the pathophysiological background for justifying RAS inhibitors as cornerstone cardiovascular protectives even during COVID-19 pandemic.Entities:
Keywords: ACE2; ADAM17; COVID-19; angiotensin II type 1 receptor blocker; angiotensin-converting enzyme inhibitor
Year: 2021 PMID: 33881142 DOI: 10.1042/CS20210182
Source DB: PubMed Journal: Clin Sci (Lond) ISSN: 0143-5221 Impact factor: 6.124