Inhibition of GSDMD Activates Poly(ADP-ribosyl)ation and Promotes Myocardial Ischemia-Reperfusion Injury.
Journal
Oxidative medicine and cellular longevity
ISSN: 1942-0994
Titre abrégé: Oxid Med Cell Longev
Pays: United States
ID NLM: 101479826
Informations de publication
Date de publication:
2022
2022
Historique:
received:
11
01
2022
revised:
03
04
2022
accepted:
15
04
2022
entrez:
5
7
2022
pubmed:
6
7
2022
medline:
7
7
2022
Statut:
epublish
Résumé
The precise control of cardiomyocyte viability is imperative to combat myocardial ischemia-reperfusion injury (I/R), in which apoptosis and pyroptosis putatively contribute to the process. Recent researches indicated that GSDMD is involved in I/R as an executive protein of pyroptosis. However, its effect on other forms of cell death is unclear. We identified that GSDMD and GSDMD-N levels were significantly upregulated in the I/R myocardium of mice. Knockout of GSDMD conferred the resistance of the hearts to reperfusion injury in the acute phase of I/R but aggravated reperfusion injury in the chronic phase of I/R. Mechanistically, GSDMD deficiency induced the activation of PARylation and the consumption of NAD
Identifiants
pubmed: 35783187
doi: 10.1155/2022/1115749
pmc: PMC9249530
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1115749Informations de copyright
Copyright © 2022 Zheng-hao Zhang et al.
Déclaration de conflit d'intérêts
The authors declare that they have no conflict of interest.
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