Metformin suppresses inflammation and apoptosis of myocardiocytes by inhibiting autophagy in a model of ischemia-reperfusion injury

Metformin (Met) is a major widely used oral glucose lowering drug for the treatment of type 2 diabetes. It is reported that metformin could regulate autophagy in various diseases of cardiovascular system including in I/R injury, diabetic cardiomyopathy and heart failure. Autophagy plays a controvers...

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Bibliographic Details
Published in:International journal of biological sciences 2020-01, Vol.16 (14), p.2559-2579
Main Authors: Huang, Kai-Yu, Que, Jia-Qun, Hu, Ze-Song, Yu, Yong-Wei, Zhou, Ying-Ying, Wang, Lei, Xue, Yang-Jing, Ji, Kang-Ting, Zhang, Xin-Min
Format: Article
Language:English
Subjects:
AKT protein
Apoptosis
Autophagy
Cardiomyocytes
Cardiomyopathy
Cardiovascular system
Congestive heart failure
Coronary vessels
CRISPR
Diabetes
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Experiments
Heart attacks
Inflammation
Injuries
Ischemia
Laboratory animals
Metformin
Phagocytosis
Reperfusion
Research Paper
Signal transduction
Surgery
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Summary:Metformin (Met) is a major widely used oral glucose lowering drug for the treatment of type 2 diabetes. It is reported that metformin could regulate autophagy in various diseases of cardiovascular system including in I/R injury, diabetic cardiomyopathy and heart failure. Autophagy plays a controversial role in ischemia/reperfusion (I/R) injury, and this research was performed to explore the cardioprotective effect of Met on I/R injury and discuss the underlying mechanism of autophagy in it. and , Met exerted cardioprotection function of decreasing myocardial inflammation and apoptosis with a decrease in the level of autophagy. Moreover, Met significantly inhibited autophagosome formation and restore the impairment of autophagosome processing, which lead to cardioprotection effect of Met. Akt was up-regulated in Met-treated I/R hearts and miransertib, a pan-AKT inhibitor, was able to reverse the alleviating autophagy effect of Met. We demonstrate that Met protects cardiomyocytes from I/R-induced apoptosis and inflammation through down regulation of autophagy mediated by Akt signaling pathway.
ISSN:1449-2288
1449-2288
DOI:10.7150/ijbs.40823