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The Protective Mechanism of Dexmedetomidine in Regulating Atg14L-Beclin1-Vps34 Complex Against Myocardial Ischemia-Reperfusion Injury.
- Source :
- Journal of Cardiovascular Translational Research; Dec2021, Vol. 14 Issue 6, p1063-1074, 12p
- Publication Year :
- 2021
-
Abstract
- The blood flow restoration of ischemic tissues causes myocardial injury. Dexmedetomidine (Dex) protects multi-organs against ischemia/reperfusion (I/R) injury. This study investigated the protective mechanism of Dex post-treatment in myocardial I/R injury. The rat model of myocardial I/R was established. The effects of Dex post-treatment on cardiac function and autophagy flow were observed. Dex attenuated myocardial I/R injury and reduced I/R-induced autophagy in rats. Dex weakened the interactions between Beclin1 and Vps34 and Beclin1 and Atg14L, thus downregulating Vps34 kinase activity. In vitro, the cardiomyocytes subjected to oxygen glucose deprivation/reoxygenation were treated with Dex and PI3K inhibitor LY294002. LY294002 attenuated the myocardial protective effect of DEX, indicating that Dex protected against cardiac I/R by activating the PI3K/Akt pathway. In conclusion, Dex upregulated the phosphorylation of Beclin1 at S295 site by activating the PI3K/Akt pathway and reduced the interactions of Atg14L-Beclin1-Vps34 complex, thus inhibiting autophagy and protecting against myocardial I/R injury. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19375387
- Volume :
- 14
- Issue :
- 6
- Database :
- Complementary Index
- Journal :
- Journal of Cardiovascular Translational Research
- Publication Type :
- Academic Journal
- Accession number :
- 153996141
- Full Text :
- https://doi.org/10.1007/s12265-021-10125-9