Mahajan Kunal, Chand Negi Prakash, Ganju Neeraj, Sondhi Sachin, Gaur Naresh, Somendra Rao
Department of Cardiology, Indira Gandhi Medical College, Shimla 171001, India.
ACE Heart and Vascular Institute, Mohali, Punjab 160062, India.
Int J Hypertens. 2020 Oct 21;2020:1025913. doi: 10.1155/2020/1025913. eCollection 2020.
The functional receptor to SARS-CoV-2, the virus responsible for the coronavirus disease 2019 (COVID-19) pandemic, is angiotensin-converting enzyme-2 (ACE-2), the same enzyme that physiologically counters the renin-angiotensin system (RAS) activation. Some researchers have questioned RAS inhibitors' safety in COVID-19 patients since these drugs have demonstrated an increase in ACE-2 expression in preclinical studies; therefore, they may facilitate viral invasion. On the contrary, others have hypothesized a protective role of RAS inhibitors against COVID-19-associated lung injury. Overall, the data are grossly inadequate to reach any conclusion since no human trials have yet evaluated the effects of RAS inhibitors in COVID-19. We review the current data and pathophysiological mechanisms behind this intriguing interplay between the RAS inhibitors and the COVID-19.
新型冠状病毒肺炎（COVID-19）大流行的病原体严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的功能性受体是血管紧张素转换酶2（ACE-2），它也是在生理上对抗肾素-血管紧张素系统（RAS）激活的同一种酶。一些研究人员质疑RAS抑制剂在COVID-19患者中的安全性，因为这些药物在临床前研究中已显示出ACE-2表达增加；因此，它们可能会促进病毒入侵。相反，其他人则假设RAS抑制剂对COVID-19相关的肺损伤具有保护作用。总体而言，由于尚无人体试验评估RAS抑制剂在COVID-19中的作用，目前的数据严重不足，无法得出任何结论。我们回顾了RAS抑制剂与COVID-19之间这种有趣相互作用背后的当前数据和病理生理机制。
