很多人不知道ACE是个啥东东， 它就是血管紧张素转化酶。想进一步了解可以看看这个文献：

https://www.frontiersin.org/articles/10.3389/fcimb.2020.00317/full

摘要谷歌翻译：

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.

严重急性呼吸系统综合症冠状病毒 (SARS-CoV-2) 感染在全球迅速蔓延，夺去了许多人的生命。 血管紧张素转化酶 2 (ACE-2) 已被确定为 SARS-CoV-2 病毒进入的受体。 因此，它现在作为抗病毒治疗的潜在靶点重新受到关注。 我们回顾了 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和抑制肺部纤维化以及保护心血管系统。 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 ACE2/MAS 通路在肺泡上皮细胞中保护作用的丧失，以及这可能如何放大肾素-血管紧张素醛固酮系统的全身性有害作用（ RAS) 在主机中。 此外，我们推测通过调节 ACE2/MAS 轴或通过开发靶向药物来抑制病毒进入所需的蛋白酶，可以利用 ACE2/MAS 通路的调节作为肺损伤的天然保护。