Mitochondrial oxidative stress induces leaky ryanodine receptor during mechanical ventilation.
Calcium homeostasis
Diaphragm contractile function
Mitochondrial oxidative stress
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
09
07
2019
revised:
28
10
2019
accepted:
15
11
2019
pubmed:
23
11
2019
medline:
22
6
2021
entrez:
23
11
2019
Statut:
ppublish
Résumé
Ventilator-induced diaphragm dysfunction (VIDD) increases morbidity and mortality in critical care patients. Although VIDD has been associated with mitochondrial oxidative stress and calcium homeostasis impairment, the underling mechanisms are still unknown. We hypothesized that diaphragmatic mitochondrial oxidative stress causes remodeling of the ryanodine receptor (RyR1)/calcium release channel, contributing to sarcoplasmic reticulum (SR) Ca In mice diaphragms mechanically ventilated for short (6 h) and long (12 h) period, we assessed mitochondrial ROS production, mitochondrial aconitase activity as a marker of mitochondrial oxidative stress, RyR1 remodeling and function, Ca 6 h of mechanical ventilation (MV) resulted in increased mitochondrial ROS production, reduction of mitochondrial aconitase activity, increased oxidation, S-nitrosylation, S-glutathionylation and Ser-2844 phosphorylation of RyR1, depletion of stabilizing subunit calstabin1 from RyR1, increased SR Ca
Identifiants
pubmed: 31756525
pii: S0891-5849(19)31137-2
doi: 10.1016/j.freeradbiomed.2019.11.019
pii:
doi:
Substances chimiques
Ryanodine Receptor Calcium Release Channel
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
383-391Informations de copyright
Copyright © 2019. Published by Elsevier Inc.