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            <name>Title</name>
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                <text>Coronavirus</text>
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                <text>Dominio científico: Coronavirus</text>
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              <text>Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers: potential allies in the COVID-19 pandemic instead of a threat?</text>
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              <text>Fedor Simko, Tomas Baka</text>
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              <text>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.</text>
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              <text>2021</text>
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              <text>covid-19, ACE2, ADAM17, angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker</text>
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              <text>10.1042/CS20210182</text>
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              <text>Clinical science (London, England : 1979)</text>
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