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...
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doaj-2437708adb844bc8acb3d4602c822c7f2021-01-20T06:48:56ZengFrontiers Media S.A.Frontiers in Medicine2296-858X2021-01-01710.3389/fmed.2020.629413629413Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 InfectionYa LiuHai-Gang ZhangThe 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.https://www.frontiersin.org/articles/10.3389/fmed.2020.629413/fullCOVID-19SARS-CoV-2atherosclerosisendothelial dysfunctioninflammationangiotensin-converting enzyme 2 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ya Liu Hai-Gang Zhang |
spellingShingle |
Ya Liu Hai-Gang Zhang Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection Frontiers in Medicine COVID-19 SARS-CoV-2 atherosclerosis endothelial dysfunction inflammation angiotensin-converting enzyme 2 |
author_facet |
Ya Liu Hai-Gang Zhang |
author_sort |
Ya Liu |
title |
Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection |
title_short |
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_sort |
vigilance on new-onset atherosclerosis following sars-cov-2 infection |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Medicine |
issn |
2296-858X |
publishDate |
2021-01-01 |
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. |
topic |
COVID-19 SARS-CoV-2 atherosclerosis endothelial dysfunction inflammation angiotensin-converting enzyme 2 |
url |
https://www.frontiersin.org/articles/10.3389/fmed.2020.629413/full |
work_keys_str_mv |
AT yaliu vigilanceonnewonsetatherosclerosisfollowingsarscov2infection AT haigangzhang vigilanceonnewonsetatherosclerosisfollowingsarscov2infection |
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