Reduced cardiac antioxidant defenses mediate increased susceptibility to workload-induced myocardial injury in males with genetic cardiomyopathy.
Angiotensin II type 1 receptor
Antioxidant
Dystrophic cardiomyopathy
Myocardial injury
S-nitrosylation
Journal
Journal of molecular and cellular cardiology
ISSN: 1095-8584
Titre abrégé: J Mol Cell Cardiol
Pays: England
ID NLM: 0262322
Informations de publication
Date de publication:
23 Mar 2024
23 Mar 2024
Historique:
received:
12
12
2023
revised:
15
03
2024
accepted:
19
03
2024
medline:
26
3
2024
pubmed:
26
3
2024
entrez:
25
3
2024
Statut:
aheadofprint
Résumé
Ongoing cardiomyocyte injury is a major mechanism in the progression of heart failure, particularly in dystrophic hearts. Due to the poor regenerative capacity of the adult heart, cardiomyocyte death results in the permanent loss of functional myocardium. Understanding the factors contributing to myocyte injury is essential for the development of effective heart failure therapies. As a model of persistent cardiac injury, we examined mice lacking β-sarcoglycan (β-SG), a key component of the dystrophin glycoprotein complex (DGC). The loss of the sarcoglycan complex markedly compromises sarcolemmal integrity in this β-SG
Identifiants
pubmed: 38527667
pii: S0022-2828(24)00044-0
doi: 10.1016/j.yjmcc.2024.03.004
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2024. Published by Elsevier Ltd.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors have no conflict of interests to declare.