Sestrin2 modulates cardiac inflammatory response through maintaining redox homeostasis during ischemia and reperfusion.
Redox Biol
; 34: 101556, 2020 07.
Article
em En
| MEDLINE
| ID: mdl-32447260
ABSTRACT
Ischemia heart disease is the leading cause of death world-widely and has increased prevalence and exacerbated myocardial infarction with aging. Sestrin2, a stress-inducible protein, declines with aging in the heart and the rescue of Sestrin2 in the aged mouse heart improves the resistance to ischemic insults caused by ischemia and reperfusion. Here, through a combination of transcriptomic, physiological, histological, and biochemical strategies, we found that Sestrin2 deficiency shows an aged-like phenotype in the heart with excessive oxidative stress, provoked immune response, and defected myocardium structure under physiological condition. While challenged with ischemia and reperfusion stress, the transcriptomic alterations in Sestrin2 knockout mouse heart resembled aged wild type mouse heart. It suggests that Sestrin2 is an age-related gene in the heart against ischemia reperfusion stress. Sestrin2 plays a crucial role in modulating inflammatory response through maintaining the intracellular redox homeostasis in the heart under ischemia reperfusion stress condition. Together, the results indicate that Sestrin2 is a potential target for treatment of age-related ischemic heart disease.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Infarto do Miocárdio
/
Miocárdio
Tipo de estudo:
Risk_factors_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article