COVID-19 pandemic is caused by the novel coronavirus SARS-CoV-2. Angiotensin-converting enzyme 2 (ACE2) is not only an enzyme but also a functional receptor on cell surfaces through which SARS-CoV-2 enters the host cells and is highly expressed in the heart, kidneys, and lungs and shed into the plasma. ACE2 is a key regulator of the renin–angiotensin–aldosterone system (RAAS). SARS-CoV-2 causes ACE/ACE2 balance disruption and RAAS activation, which leads ultimately to COVID-19 progression, especially in patients with comorbidities, such as hypertension, diabetes mellitus, and cardiovascular disease. Therefore, ACE2 expression may have paradoxical effects, aiding SARS-CoV-2 pathogenicity, yet conversely limiting viral infection. This article reviews the existing literature and knowledge of ACE2 in COVID-19 setting and focuses on its pathophysiologic involvement in disease progression, clinical outcomes, and therapeutic potential.

COVID-19 大流行是由新型冠状病毒 SARS-CoV-2 引起的。血管紧张素转换酶2（ACE2）不仅是一种酶，也是细胞表面的功能性受体，SARS-CoV-2通过它进入宿主细胞，在心脏、肾脏和肺中高度表达并流入血浆。 ACE2 是肾素-血管紧张素-醛固酮系统 (RAAS) 的关键调节因子。 SARS-CoV-2 会导致 ACE/ACE2 平衡破坏和 RAAS 激活，最终导致 COVID-19 进展，尤其是患有高血压、糖尿病和心血管疾病等合并症的患者。因此，ACE2 表达可能具有矛盾的作用，有助于 SARS-CoV-2 的致病性，但反过来又限制病毒感染。本文回顾了 ACE2 在 COVID-19 背景下的现有文献和知识，重点关注其在疾病进展、临床结果和治疗潜力中的病理生理学参与。