Cited by 897Renin-Angiotensin System StudiesSARS-CoV-2 and COVID-19 ResearchCOVID-19 Clinical Research Studies

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

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Beyerstedt, Stephany, Casaro, Expedito Barbosa, Rangel, Érika Bevilaqua·2021·European Journal of Clinical Microbiology & Infectious Diseases

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.

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  • ACE2 on endothelial cells of the arteries, arterioles, and venules of the heart and kidney determines its ability to regulate vascular function and blood pressure.

    “ACE2 on endothelial cells of the arteries, arterioles, and venules of the heart and kidney determines its ability to regulate vascular function and blood pressure, as reviewed previously.”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [54]

    The section on ACE2 and the renin–angiotensin–aldosterone system (page unavailable) says ACE2 helps regulate haemodynamics and lowers blood pressure through vasodilation. The Comorbidities section (page unavailable) reports ACE2 expression in the heart, kidneys, and cardiac endothelial cells. Neither passage establishes the claim's specific localization to endothelial cells of arteries, arterioles, and venules in both organs. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Beyerstedt, S., Casaro, E. B., & Rangel, É. B.
Affiliations
Hospital Israelita Albert Einstein (BR)
Corresponding author
Rangel, Érika Bevilaqua
Venue
European Journal of Clinical Microbiology & Infectious Diseases
Published
2021-01-03
Volume
40
Issue
5
Pages
905-919
ISSN
  • 0934-9723 (ISSN-L)
  • 1435-4373
OpenAlex
W3118438588
Cited by
897
References
16
Citations by year
2026: 54 · 2025: 118 · 2024: 184 · 2023: 235 · 2022: 223 · 2021: 76 · 2020: 2 · 2019: 1 · 2018: 3
FWCI
35.09
Type
journal article
Language
en
Open access
Locations
  • European Journal of Clinical Microbiology & Infectious Diseases (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
FAPESP (2017/23195-2)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
  • Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
Keywords
COVID-19 pandemic, SARS-CoV-2, angiotensin-converting enzyme 2, ACE2 expression, renin-angiotensin-aldosterone system, viral entry receptor, hypertension, diabetes mellitus, cardiovascular disease, comorbidities, disease progression, therapeutic target
MeSH terms
Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Antibodies, Monoclonal, Humans, Peptidyl-Dipeptidase A, Polymorphism, Genetic, Renin-Angiotensin System, Comorbidity, Spike Glycoprotein, Coronavirus

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