COVID-19: angiotensin-converting enzyme 2 (ACE2) expression and tissue susceptibility to SARS-CoV-2 infection

被引：540

作者：

Beyerstedt, Stephany ^{[1
]}

Casaro, Expedito Barbosa ^{[1
]}

Rangel, Erika Bevilaqua ^{[1
,2
]}

机构：

[1] Hosp Israelita Albert Einstein, Albert Einstein Res & Educ Inst, 627 Albert Einstein Ave,Bldg A, Sao Paulo, SP, Brazil

[2] Univ Fed Sao Paulo, Nephrol Div, Sao Paulo, SP, Brazil

来源：

EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES | 2021年 / 40卷 / 05期

基金：

巴西圣保罗研究基金会;

关键词：

Angiotensin-converting enzyme; COVID-19; SARS-CoV-2; Tissue damage; ALDOSTERONE SYSTEM INHIBITORS; KALLIKREIN-KININ SYSTEM; DIABETES-MELLITUS; EPITHELIAL-CELLS; RECEPTOR ACE2; CORONAVIRUS; MORTALITY; TMPRSS2; HYPERTENSION; POLYMORPHISM;

D O I：

10.1007/s10096-020-04138-6

中图分类号：

R51 [传染病];

学科分类号：

100401 ;

摘要：

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.

引用

页码：905 / 919

页数：15

共 152 条

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