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Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection
The pandemic of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has become a global challenge to public health. While its typical clinical manifestations are respiratory disorders, emerging evidence of cardiovascular complications indicates the adverse interaction between SARS-CoV-2 infec...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7855580/ https://www.ncbi.nlm.nih.gov/pubmed/33553222 http://dx.doi.org/10.3389/fmed.2020.629413 |
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author | Liu, Ya Zhang, Hai-Gang |
author_facet | Liu, Ya Zhang, Hai-Gang |
author_sort | Liu, Ya |
collection | PubMed |
description | The pandemic of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has become a global challenge to public health. While its typical clinical manifestations are respiratory disorders, emerging evidence of cardiovascular complications indicates the adverse interaction between SARS-CoV-2 infection and cardiovascular outcomes. Given that viral infection has emerged as an additional risk factor for atherosclerosis, in this paper, we attempt to clarify the susceptibility to new-onset atherosclerosis in individuals infected with SARS-CoV-2. Mechanistically, serving as functional receptors for SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2) mediates SARS-CoV-2 infection of endothelial cells (ECs) directly, leading to endothelial dysfunction and dysregulation of the renin-angiotensin system (RAS). In addition, high expression of CD147, an alternative receptor, and activation of the NLRP3 inflammasome may also contribute to atherosclerosis in the context of COVID-19. More importantly, SARS-CoV-2 attacks the immune system, which results in excessive inflammation and perpetuates a vicious cycle of deteriorated endothelial dysfunction that further promotes inflammation. The alterations in the blood lipid profile induced by COVID-19 should not be ignored in assessing the predisposition toward atherosclerosis in victims of COVID-19. A better understanding of the underlying mechanisms of SARS-CoV-2 infection and the long-term monitoring of inflammatory factors and endothelial function should be considered in the follow-up of patients who have recovered from COVID-19 for early detection and prevention of atherosclerosis. |
format | Online Article Text |
id | pubmed-7855580 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78555802021-02-04 Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection Liu, Ya Zhang, Hai-Gang Front Med (Lausanne) Medicine The pandemic of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has become a global challenge to public health. While its typical clinical manifestations are respiratory disorders, emerging evidence of cardiovascular complications indicates the adverse interaction between SARS-CoV-2 infection and cardiovascular outcomes. Given that viral infection has emerged as an additional risk factor for atherosclerosis, in this paper, we attempt to clarify the susceptibility to new-onset atherosclerosis in individuals infected with SARS-CoV-2. Mechanistically, serving as functional receptors for SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2) mediates SARS-CoV-2 infection of endothelial cells (ECs) directly, leading to endothelial dysfunction and dysregulation of the renin-angiotensin system (RAS). In addition, high expression of CD147, an alternative receptor, and activation of the NLRP3 inflammasome may also contribute to atherosclerosis in the context of COVID-19. More importantly, SARS-CoV-2 attacks the immune system, which results in excessive inflammation and perpetuates a vicious cycle of deteriorated endothelial dysfunction that further promotes inflammation. The alterations in the blood lipid profile induced by COVID-19 should not be ignored in assessing the predisposition toward atherosclerosis in victims of COVID-19. A better understanding of the underlying mechanisms of SARS-CoV-2 infection and the long-term monitoring of inflammatory factors and endothelial function should be considered in the follow-up of patients who have recovered from COVID-19 for early detection and prevention of atherosclerosis. Frontiers Media S.A. 2021-01-20 /pmc/articles/PMC7855580/ /pubmed/33553222 http://dx.doi.org/10.3389/fmed.2020.629413 Text en Copyright © 2021 Liu and Zhang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Medicine Liu, Ya Zhang, Hai-Gang Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title | Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_full | Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_fullStr | Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_full_unstemmed | Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_short | Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_sort | vigilance on new-onset atherosclerosis following sars-cov-2 infection |
topic | Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7855580/ https://www.ncbi.nlm.nih.gov/pubmed/33553222 http://dx.doi.org/10.3389/fmed.2020.629413 |
work_keys_str_mv | AT liuya vigilanceonnewonsetatherosclerosisfollowingsarscov2infection AT zhanghaigang vigilanceonnewonsetatherosclerosisfollowingsarscov2infection |