Protective role of the mitochondrial fusion protein OPA1 in hypertension.
Animals
Apoptosis
Enzyme Inhibitors
/ toxicity
GTP Phosphohydrolases
/ physiology
Hypertension
/ chemically induced
Male
Mice, Inbred C57BL
Mice, Knockout
Mitochondrial Dynamics
NG-Nitroarginine Methyl Ester
/ toxicity
Oxidative Stress
Protective Agents
/ administration & dosage
Reactive Oxygen Species
/ metabolism
Opa1
hypertension
mitochondria
oxidative stress
vascular function
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
revised:
04
05
2021
received:
17
02
2020
accepted:
04
05
2021
entrez:
16
6
2021
pubmed:
17
6
2021
medline:
20
7
2021
Statut:
ppublish
Résumé
Hypertension is associated with excessive reactive oxygen species (ROS) production in vascular cells. Mitochondria undergo fusion and fission, a process playing a role in mitochondrial function. OPA1 is essential for mitochondrial fusion. Loss of OPA1 is associated with ROS production and cell dysfunction. We hypothesized that mitochondria fusion could reduce oxidative stress that defect in fusion would exacerbate hypertension. Using (a) Opa1 haploinsufficiency in isolated resistance arteries from Opa1
Identifiants
pubmed: 34133045
doi: 10.1096/fj.202000238RRR
doi:
Substances chimiques
Enzyme Inhibitors
0
Protective Agents
0
Reactive Oxygen Species
0
GTP Phosphohydrolases
EC 3.6.1.-
Opa1 protein, mouse
EC 3.6.1.-
NG-Nitroarginine Methyl Ester
V55S2QJN2X
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e21678Informations de copyright
© 2021 Federation of American Societies for Experimental Biology.
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