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Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible virus with significant global impact, morbidity, and mortality. The SARS-CoV-2 virus may result in widespread organ manifestations including acute respiratory distress syndrome, acute renal failure, thromboemb...

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Autores principales: Prasad, Megha, Leon, Martin, Lerman, Lilach O., Lerman, Amir
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier Inc on behalf of Mayo Foundation for Medical Education and Research 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8373818/
https://www.ncbi.nlm.nih.gov/pubmed/34863398
http://dx.doi.org/10.1016/j.mayocp.2021.06.027
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author Prasad, Megha
Leon, Martin
Lerman, Lilach O.
Lerman, Amir
author_facet Prasad, Megha
Leon, Martin
Lerman, Lilach O.
Lerman, Amir
author_sort Prasad, Megha
collection PubMed
description The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible virus with significant global impact, morbidity, and mortality. The SARS-CoV-2 virus may result in widespread organ manifestations including acute respiratory distress syndrome, acute renal failure, thromboembolism, and myocarditis. Virus-induced endothelial injury may cause endothelial activation, increased permeability, inflammation, and immune response and cytokine storm. Endothelial dysfunction is a systemic disorder that is a precursor of atherosclerotic vascular disease that is associated with cardiovascular risk factors and is highly prevalent in patients with atherosclerotic cardiovascular and peripheral disease. Several studies have associated various viral infections including SARS-CoV-2 infection with inflammation, endothelial dysfunction, and subsequent innate immune response and cytokine storm. Noninvasive monitoring of endothelial function and identification of high-risk patients who may require specific therapies may have the potential to improve morbidity and mortality associated with subsequent inflammation, cytokine storm, and multiorgan involvement.
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spelling pubmed-83738182021-08-19 Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19 Prasad, Megha Leon, Martin Lerman, Lilach O. Lerman, Amir Mayo Clin Proc Review The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible virus with significant global impact, morbidity, and mortality. The SARS-CoV-2 virus may result in widespread organ manifestations including acute respiratory distress syndrome, acute renal failure, thromboembolism, and myocarditis. Virus-induced endothelial injury may cause endothelial activation, increased permeability, inflammation, and immune response and cytokine storm. Endothelial dysfunction is a systemic disorder that is a precursor of atherosclerotic vascular disease that is associated with cardiovascular risk factors and is highly prevalent in patients with atherosclerotic cardiovascular and peripheral disease. Several studies have associated various viral infections including SARS-CoV-2 infection with inflammation, endothelial dysfunction, and subsequent innate immune response and cytokine storm. Noninvasive monitoring of endothelial function and identification of high-risk patients who may require specific therapies may have the potential to improve morbidity and mortality associated with subsequent inflammation, cytokine storm, and multiorgan involvement. Published by Elsevier Inc on behalf of Mayo Foundation for Medical Education and Research 2021-12 2021-08-19 /pmc/articles/PMC8373818/ /pubmed/34863398 http://dx.doi.org/10.1016/j.mayocp.2021.06.027 Text en © 2021 Published by Elsevier Inc on behalf of Mayo Foundation for Medical Education and Research. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Review
Prasad, Megha
Leon, Martin
Lerman, Lilach O.
Lerman, Amir
Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title_full Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title_fullStr Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title_full_unstemmed Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title_short Viral Endothelial Dysfunction: A Unifying Mechanism for COVID-19
title_sort viral endothelial dysfunction: a unifying mechanism for covid-19
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8373818/
https://www.ncbi.nlm.nih.gov/pubmed/34863398
http://dx.doi.org/10.1016/j.mayocp.2021.06.027
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