TIPE2 protects cardiomyocytes from ischemia‑reperfusion‑induced apoptosis by decreasing cell autophagy via the mTORC1 signaling pathway
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- Published online on: August 4, 2022 https://doi.org/10.3892/etm.2022.11550
- Article Number: 613
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Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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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‑α‑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.