Institute of Pathophysiology, Faculty of Medicine, Comenius University, Bratislava 81108, Slovak Republic.
Third Department of Internal Medicine, Faculty of Medicine, Comenius University, Bratislava 83305, Slovak Republic.
Clin Sci (Lond). 2021 Apr 30;135(8):1009-1014. doi: 10.1042/CS20210182.
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.
血管紧张素转换酶 2(ACE2)是保护性肾素-血管紧张素系统(RAS)途径的主要参与者,但也是严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)的进入受体。RAS 抑制剂似乎会干扰 ACE2 受体,其在 COVID-19 患者中的安全性已得到解决。Pedrosa 等人(Clin. Sci. (Lond.) (2021),135,465-481)在大鼠中表明,卡托普利和坎地沙坦可上调肺组织中的 ACE2 表达和保护性 RAS 途径。在肺细胞培养物中,卡托普利/坎地沙坦诱导的 ACE2 上调与 ADAM17 活性的抑制有关,抵消了 ACE2 表达的增加,这与 SARS-CoV-2 刺突蛋白进入减少有关。如果在人类中得到证实,这些结果可能成为将 RAS 抑制剂作为心血管保护基石的病理生理学基础,即使在 COVID-19 大流行期间也是如此。