Journal
EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
Volume 40, Issue 5, Pages 905-919Publisher
SPRINGER
DOI: 10.1007/s10096-020-04138-6
Keywords
Angiotensin-converting enzyme; COVID-19; SARS-CoV-2; Tissue damage
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Funding
- FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo/Sao Paulo Research Foundation) [2017/23195-2]
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ACE2 plays a crucial role in COVID-19, with its expression potentially having paradoxical effects, aiding SARS-CoV-2 pathogenicity while also limiting viral infection.
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.
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