Division of Pediatric Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, 70112, USA.
Nat Commun. 2020 Oct 14;11(1):5165. doi: 10.1038/s41467-020-18880-0.
Angiotensin-converting enzyme 2 (ACE2) has been identified as the host entry receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) responsible for the COVID-19 pandemic. ACE2 is a regulatory enzyme of the renin-angiotensin system and has protective functions in many cardiovascular, pulmonary and metabolic diseases. This review summarizes available murine models with systemic or organ-specific deletion of ACE2, or with overexpression of murine or human ACE2. The purpose of this review is to provide researchers with the genetic tools available for further understanding of ACE2 biology and for the investigation of ACE2 in the pathogenesis and treatment of COVID-19.
血管紧张素转换酶 2（ACE2）已被确定为导致 COVID-19 大流行的严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）的宿主进入受体。ACE2 是肾素-血管紧张素系统的调节酶，在许多心血管、肺部和代谢疾病中具有保护作用。这篇综述总结了具有全身性或器官特异性 ACE2 缺失或过表达鼠或人 ACE2 的可用小鼠模型。本综述的目的是为研究人员提供可用的遗传工具，以进一步了解 ACE2 生物学，并研究 ACE2 在 COVID-19 的发病机制和治疗中的作用。
