Division of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PT, U.K.
School of Clinical Dentistry and Neuroscience Institute, University of Sheffield, Sheffield S10 2TA, U.K.
Clin Sci (Lond). 2020 Sep 30;134(18):2489-2501. doi: 10.1042/CS20200476.
Angiotensin-converting enzyme (ACE) is a zinc membrane metallopeptidase that plays a key role in regulating vasoactive peptide levels and hence cardiovascular activity through its conversion of angiotensin I (Ang I) to Ang II and its metabolism of bradykinin. The discovery of its homologue, ACE2, 20 years ago has led to intensive comparisons of these two enzymes revealing surprising structural, catalytic and functional distinctions between them. ACE2 plays multiple roles not only as a vasopeptidase but also as a regulator of amino acid transport and serendipitously as a viral receptor, mediating the cellular entry of the coronaviruses causing severe acute respiratory syndrome (SARS) and, very recently, COVID-19. Catalytically, ACE2 functions as a monocarboxypeptidase principally converting the vasoconstrictor angiotensin II to the vasodilatory peptide Ang-(1-7) thereby counterbalancing the action of ACE on the renin-angiotensin system (RAS) and providing a cardioprotective role. Unlike ACE, ACE2 does not metabolise bradykinin nor is it inhibited by classical ACE inhibitors. However, it does convert a number of other regulatory peptides in vitro and in vivo. Interest in ACE2 biology and its potential as a possible therapeutic target has surged in recent months as the COVID-19 pandemic rages worldwide. This review highlights the surprising discoveries of ACE2 biology during the last 20 years, its distinctions from classical ACE and the therapeutic opportunities arising from its multiple biological roles.
血管紧张素转换酶(ACE)是一种锌膜金属肽酶,通过将血管紧张素 I(Ang I)转化为血管紧张素 II 并代谢缓激肽,在调节血管活性肽水平从而影响心血管活动方面发挥着关键作用。20 年前发现其同源物 ACE2 后,人们对这两种酶进行了深入比较,揭示了它们在结构、催化和功能方面令人惊讶的差异。ACE2 不仅作为血管肽酶发挥多种作用,还作为氨基酸转运调节剂,以及冠状病毒的意外受体,介导引起严重急性呼吸系统综合征(SARS)的冠状病毒和最近的 COVID-19 进入细胞。在催化方面,ACE2 作为单羧肽酶起作用,主要将血管收缩肽血管紧张素 II 转化为血管舒张肽 Ang-(1-7),从而抵消 ACE 对肾素-血管紧张素系统(RAS)的作用,并发挥心脏保护作用。与 ACE 不同,ACE2 不代谢缓激肽,也不受经典 ACE 抑制剂的抑制。然而,它确实在体外和体内转化了许多其他调节肽。随着 COVID-19 大流行在全球肆虐,近几个月来,人们对 ACE2 生物学及其作为可能的治疗靶点的潜力产生了浓厚兴趣。本文综述了过去 20 年来 ACE2 生物学的惊人发现,及其与经典 ACE 的区别以及其多种生物学作用带来的治疗机会。