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

Author(s)

Beyerstedt, Stephany ^[1] ; Casaro, Expedito Barbosa ^[1] ; Rangel, Erika Bevilaqua ^{[2, 1]}

Affiliation

^[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

• Document type: Review article
• Source: EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES; v. 40, n. 5 JAN 2021.
• Web of Science Citations: 6

Abstract

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. (AU)

• FAPESP's process: 17/23195-2 - Mesenchymal stem cell therapy for halting the progression of acute and chronic kidney injury and in vivo modulate kidney-derived c-Kit stem cells
• Grantee: Érika Bevilaqua Rangel
• Support Opportunities: Regular Research Grants