TIPE2 protects cardiomyocytes from ischemia-reperfusion-induced apoptosis by decreasing cell autophagy via the mTORC1 signaling pathway
EXPERIMENTAL AND THERAPEUTIC MEDICINE(2022)
Abstract
In cardiac ischemia-reperfusion (I/R), autophagy of hyperactivated cardiomyocytes degrades normal proteins and organelles, destroys cells and causes irreversible cell death. The present study aimed to determine the molecular mechanism through which TNF-alpha-induced protein 8-like protein 2 (TIPE2) regulates cardiomyocyte apoptosis via autophagy in I/R. The results revealed that the number of apoptotic cells and the protein expression levels of TIPE2 in the heart tissue of I/R model mice were significantly increased. In vitro, the overexpression of TIPE2 decreased oxygen glucose deprivation (OGD)-induced autophagy, apoptosis and activation of the mTOR complex 1 (mTORC1) signaling pathway in H9c2 cells. Treatment with the mTORC1 inhibitor not only inhibited the TIPE2-activated mTORC1 signaling pathway, but also increased OGD-induced autophagy and apoptosis of H9c2 cells. In conclusion, the results of the present study revealed that TIPE2 may protect cardiomyocytes from I/R-induced apoptosis by decreasing cell autophagy via the mTORC1 signaling pathway.
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Key words
TNF-alpha-induced protein 8-like protein 2, mTOR complex 1, autophagy
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