TRAF5 protects against myocardial ischemia reperfusion injury via AKT signaling.
Eur J Pharmacol
; 878: 173092, 2020 Jul 05.
Article
in En
| MEDLINE
| ID: mdl-32234528
During the processes of myocardial ischemia reperfusion (I/R) injury, inflammation and apoptosis play an important role. I/R and its induced acute myocardial infarction (AMI) with high morbidity and mortality, and there is no effective treatment for it so far. TRAF5 has been shown to regulate inflammation and apoptosis in atherosclerosis, steatosis and melanoma cells, but its function in myocardial I/R injury is still unclear. This study demonstrates that the expression of TRAF5 is significant up-regulation in heart tissues of I/R injury mice and hypoxia/reoxygenation (H/R)-stimulated cardiomyocytes. TRAF5 knockout mice exhibites heavier heart damage, inflammatory response and cell death after myocardial I/R injury. Further, TRAF5 overexpression inhibites inflammation and apoptosis of H/R-stimulated cardiomyocytes. Mechanistically, we prove that TRAF5 promotes the activation of AKT. Overall, our study indicates that TRAF5 can regulate the processes of myocardial I/R injury. TRAF5 can be a new therapy target for myocardial I/R injury.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Myocardial Reperfusion Injury
/
Protective Agents
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TNF Receptor-Associated Factor 5
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Proto-Oncogene Proteins c-akt
Limits:
Animals
/
Humans
Language:
En
Journal:
Eur J Pharmacol
Year:
2020
Document type:
Article
Affiliation country:
China
Country of publication:
Netherlands