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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Published inFrontiers in medicine Vol. 7; p. 629413
Main Authors Liu, Ya, Zhang, Hai-Gang
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 20.01.2021
Subjects
angiotensin-converting enzyme 2
atherosclerosis
COVID-19
endothelial dysfunction
inflammation
Medicine
SARS-CoV-2
COVID-19
atherosclerosis
SARS-CoV-2
angiotensin-converting enzyme 2
inflammation
endothelial dysfunction
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Abstract 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.
AbstractList 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.
Author Zhang, Hai-Gang
Liu, Ya
AuthorAffiliation Department of Pharmacology, College of Pharmacy, Army Medical University (Third Military Medical University) , Chongqing , China
AuthorAffiliation_xml – name: Department of Pharmacology, College of Pharmacy, Army Medical University (Third Military Medical University) , Chongqing , China
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  givenname: Ya
  surname: Liu
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  givenname: Hai-Gang
  surname: Zhang
  fullname: Zhang, Hai-Gang
  organization: Department of Pharmacology, College of Pharmacy, Army Medical University (Third Military Medical University), Chongqing, China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33553222$$D View this record in MEDLINE/PubMed
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Keywords COVID-19
atherosclerosis
SARS-CoV-2
angiotensin-converting enzyme 2
inflammation
endothelial dysfunction
Language English
License Copyright © 2021 Liu and Zhang.
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.
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This article was submitted to Infectious Diseases - Surveillance, Prevention and Treatment, a section of the journal Frontiers in Medicine
Reviewed by: Aris P. Agouridis, German Oncology Center, Cyprus; Pedro Xavier-Elsas, Federal University of Rio de Janeiro, Brazil
Edited by: Constantinos Tsioutis, European University Cyprus, Cyprus
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Snippet 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...
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SubjectTerms angiotensin-converting enzyme 2
atherosclerosis
COVID-19
endothelial dysfunction
inflammation
Medicine
SARS-CoV-2
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Title Vigilance on New-Onset Atherosclerosis Following SARS-CoV-2 Infection
URI https://www.ncbi.nlm.nih.gov/pubmed/33553222
https://search.proquest.com/docview/2487432311
https://pubmed.ncbi.nlm.nih.gov/PMC7855580
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Volume 7
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