期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 16, 期 14, 页码 2559-2579出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.40823
关键词
Metformin; autophagy; apoptosis; inflammation; myocardial ischemia reperfusion
资金
- National Natural Science Foundation of China [81573185, 17331201, 18331207]
- Wenzhou Municipal Science and Technology Bureau [H20140003, Y20140678, Y20170253]
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. In vivo and in vitro, 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.
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