Abstract |
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.
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Authors | Weipan Xu, Li Zhang, Shanxue Ma, Yi Zhang, Zhenxuan Cai, Kai Zhang, Daoqun Jin |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 878
Pg. 173092
(Jul 05 2020)
ISSN: 1879-0712 [Electronic] Netherlands |
PMID | 32234528
(Publication Type: Journal Article)
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Copyright | Copyright © 2020 Elsevier B.V. All rights reserved. |
Chemical References |
- Protective Agents
- Recombinant Proteins
- TNF Receptor-Associated Factor 5
- Proto-Oncogene Proteins c-akt
|
Topics |
- Animals
- Apoptosis
- HEK293 Cells
- Humans
- Hypoxia
(metabolism)
- Inflammation
- Lentivirus
(genetics)
- Mice, Knockout
- Molecular Targeted Therapy
- Myocardial Infarction
(drug therapy)
- Myocardial Reperfusion Injury
(drug therapy, prevention & control)
- Myocytes, Cardiac
(metabolism)
- Protective Agents
(metabolism)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Recombinant Proteins
(genetics, metabolism)
- Signal Transduction
- TNF Receptor-Associated Factor 5
(genetics, metabolism)
- Transfection
- Up-Regulation
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