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.
【저자키워드】 COVID-19, ACE2, ADAM17, angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker, 【초록키워드】 SARS-CoV-2, coronavirus, COVID-19 pandemic, ACE2 receptor, RAS, Culture, humans, SARS-CoV-2 spike protein, pathway, ACE2 expression, COVID-19 patients, Protective, Pneumocytes, candesartan, acute respiratory syndrome, enzyme, lung tissue, entry receptor, Clin, reduced, interfere, up-regulated, addressed, pathophysiological, RAS inhibitor, 【제목키워드】 COVID-19 pandemic, receptor, inhibitor, enzyme,