Altered mitochondrial quality control in Atg7-deficient VSMCs promotes enhanced apoptosis and is linked to unstable atherosclerotic plaque phenotype.
Animals
Apolipoproteins E
/ deficiency
Apoptosis
Autophagy-Related Protein 7
/ deficiency
Cells, Cultured
Membrane Potential, Mitochondrial
Mice
Mice, Knockout
Mitochondria
/ metabolism
Mitophagy
Muscle, Smooth, Vascular
/ cytology
Oxidative Stress
Plaque, Atherosclerotic
/ metabolism
Reactive Oxygen Species
/ metabolism
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
11 02 2019
11 02 2019
Historique:
received:
02
10
2018
accepted:
29
01
2019
revised:
28
01
2019
entrez:
12
2
2019
pubmed:
12
2
2019
medline:
13
2
2020
Statut:
epublish
Résumé
Vascular smooth muscle cells (VSMCs) are one of the main cellular determinants in arterial pathology. A large body of evidence indicates that death of VSMCs is associated with features of high-risk/vulnerable atherosclerotic plaques. Mitochondrial turnover is an essential aspect of the mitochondrial quality control in which dysfunctional mitochondria are selectively eliminated through autophagy and replaced through expansion of preexisting mitochondria. Even though successful autophagy promotes VSMC survival, it is unclear whether reduced autophagic flux affects mitochondrial quality control of VSMCs in atherosclerotic plaques. By using apolipoprotein E-deficient (ApoE
Identifiants
pubmed: 30741928
doi: 10.1038/s41419-019-1400-0
pii: 10.1038/s41419-019-1400-0
pmc: PMC6370858
doi:
Substances chimiques
Apolipoproteins E
0
Reactive Oxygen Species
0
Autophagy-Related Protein 7
EC 6.2.1.45
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
119Références
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