The Renin-Angiotensin-Aldosterone System and Coronavirus Disease 2019.

COVID-19 SARS-CoV-2 angiotensin II receptor inhibitors angiotensin-converting enzyme inhibitors angiotensin-converting enzyme polymorphisms cardiovascular comorbidities coronavirus renin–angiotensin–aldosterone system

Journal

European cardiology
ISSN: 1758-3764
Titre abrégé: Eur Cardiol
Pays: England
ID NLM: 101574780

Informations de publication

Date de publication:
Feb 2021
Historique:
received: 04 06 2020
accepted: 10 10 2020
entrez: 19 3 2021
pubmed: 20 3 2021
medline: 20 3 2021
Statut: epublish

Résumé

The renin-aldosterone-angiotensin system (RAAS) plays an important role in the pathogenesis of coronavirus disease 2019 (COVID-19), which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV-2 and the host's expression of this membrane-bound protein could affect susceptibility to infection. The RAAS is an important regulator of cardiovascular physiology and ACE2 has an essential role. People with hypertension and other traits have shown to have an imbalance in ACE/ACE2 levels and reduced levels of ACE2 could enhance the risk of adverse outcome in patients with COVID-19. It has been hypothesised that the RAAS may mediate the interplay between cardiovascular disease and COVID-19 severity. Evidence shows that antihypertensive drugs that target the RAAS have no significant effect on the risk of infection and disease outcome. Variations in RAAS genes have been associated with the risk of developing hypertension and cardiovascular disease and could partly explain the heterogenous response to SARS-CoV-2 infection. This article explores the interplay between the RAAS and COVID-19, with emphasis on the possible relationship between genetic variations and disease severity.

Identifiants

pubmed: 33737961
doi: 10.15420/ecr.2020.30
pmc: PMC7967817
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

e07

Informations de copyright

Copyright © 2021, Radcliffe Cardiology.

Déclaration de conflit d'intérêts

Disclosure: This work was supported by a grant from the Spanish Plan Nacional de Investigación Científica, Desarrollo e Innovación Tecnológica, Ministerio de Economía y Competitividad and a grant from the European Regional Development Fund (ISCIII-Red de Investigación Renal-REDINREN RD16/9/5 [EC]). The authors have no other conflicts of interest to disclose.

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Auteurs

Eliecer Coto (E)

Genética Molecular, Hospital Universitario Central Asturias Oviedo, Spain.
Instituto de Investigación Sanitaria del Principado de Asturias, ISPA Oviedo, Spain.
Universidad de Oviedo Oviedo, Spain.
Red de Investigación Renal (REDINREN) Madrid, Spain.

Pablo Avanzas (P)

Cardiología, Hospital Universitario Central Asturias Oviedo, Spain.
Instituto de Investigación Sanitaria del Principado de Asturias, ISPA Oviedo, Spain.
Universidad de Oviedo Oviedo, Spain.

Juan Gómez (J)

Genética Molecular, Hospital Universitario Central Asturias Oviedo, Spain.
Instituto de Investigación Sanitaria del Principado de Asturias, ISPA Oviedo, Spain.

Classifications MeSH