The rapidly evolving pandemic of severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection worldwide cost many lives. The angiotensin converting enzyme-2 (ACE-2) has been identified as the receptor for the SARS-CoV-2 viral entry. As such, it is now receiving renewed attention as a potential target for anti-viral therapeutics. We review the physiological functions of ACE2 in the cardiovascular system and the lungs, and how the activation of ACE2/MAS/G protein coupled receptor contributes in reducing acute injury and inhibiting fibrogenesis of the lungs and protecting the cardiovascular system. In this perspective, we predominantly focus on the impact of SARS-CoV-2 infection on ACE2 and dysregulation of the protective effect of ACE2/MAS/G protein pathway vs. the deleterious effect of Renin/Angiotensin/Aldosterone. We discuss the potential effect of invasion of SARS-CoV-2 on the function of ACE2 and the loss of the protective effect of the ACE2/MAS pathway in alveolar epithelial cells and how this may amplify systemic deleterious effect of renin-angiotensin aldosterone system (RAS) in the host. Furthermore, we speculate the potential of exploiting the modulation of ACE2/MAS pathway as a natural protection of lung injury by modulation of ACE2/MAS axis or by developing targeted drugs to inhibit proteases required for viral entry.

严重急性呼吸综合征冠状病毒 (SARS-CoV-2) 感染在全球范围内迅速蔓延，夺去了许多人的生命。血管紧张素转换酶 2 (ACE-2) 已被确定为 SARS-CoV-2 病毒进入的受体。因此，它作为抗病毒治疗的潜在靶点现在重新受到关注。我们综述了ACE2在心血管系统和肺部的生理功能，以及ACE2/MAS/G蛋白偶联受体的激活如何有助于减少急性损伤、抑制肺部纤维形成、保护心血管系统。从这个角度来看，我们主要关注 SARS-CoV-2 感染对 ACE2 的影响，以及 ACE2/MAS/G 蛋白通路的保护作用与肾素/血管紧张素/醛固酮的有害作用的失调。我们讨论了 SARS-CoV-2 入侵对 ACE2 功能的潜在影响以及肺泡上皮细胞中 ACE2/MAS 通路保护作用丧失的潜在影响，以及这如何放大肾素-血管紧张素醛固酮系统的全身有害作用。 RAS）在主机中。此外，我们推测通过调节 ACE2/MAS 轴或开发靶向药物来抑制病毒进入所需的蛋白酶，利用 ACE2/MAS 途径的调节作为肺损伤的自然保护的潜力。