Severe acute respiratory syndrome coronaviruses contributing to mitochondrial dysfunction: Implications for post-COVID complications.
CoV
Mitochondria
Mitochondrial localization signal
ROS
SARS
Virus
Journal
Mitochondrion
ISSN: 1872-8278
Titre abrégé: Mitochondrion
Pays: Netherlands
ID NLM: 100968751
Informations de publication
Date de publication:
03 2023
03 2023
Historique:
received:
09
07
2022
revised:
03
01
2023
accepted:
03
01
2023
pubmed:
24
1
2023
medline:
14
3
2023
entrez:
23
1
2023
Statut:
ppublish
Résumé
Mitochondria play a central role in oxidative phosphorylation (OXPHOS), bioenergetics linked with ATP production, fatty acids biosynthesis, calcium signaling, cell cycle regulation, apoptosis, and innate immune response. Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection manipulates the host cellular machinery for its survival and replication in the host cell. The infectiaon causes perturbed the cellular metabolism that favours viral replication leading to mitochondrial dysfunction and chronic inflammation. By localizing to the mitochondria, SARS CoV proteins increase reactive oxygen species (ROS) levels, perturbation of Ca
Identifiants
pubmed: 36690315
pii: S1567-7249(23)00005-3
doi: 10.1016/j.mito.2023.01.005
pmc: PMC9854144
pii:
doi:
Substances chimiques
DNA, Mitochondrial
0
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
43-56Informations de copyright
Copyright © 2023 Elsevier B.V. and Mitochondria Research Society. All rights reserved. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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