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• W2951236951 endingPage "116560" @default.
• W2951236951 startingPage "116560" @default.
• W2951236951 abstract "Mitochondrial dysfunction caused by calcium overload is a vital factor for mediating cardiomyocyte death following ischemia/reperfusion (I/R) injury. The stromal interactive molecule 2 (STIM2) is a calcium sensor protein that regulates the store-operated calcium entry (SOCE). Whereas, whether STIM2 is associated with I/R injury remains largely unclear. We report here that STIM2, but not its homologue STIM1, is upregulated in cultured H9c2 cells, a cell model for cardiomyocytes, following I/R injury. In addition, the knockdown of STIM2, but not STIM1, reduces H9c2 cell apoptosis following I/R injury, and similar results were obtained in primary neonatal cardiomyocytes. This anti-apoptotic effect could be attributed to the inhibited activation of mitochondrial apoptosis pathway. Moreover, STIM2 knockdown reduces ER calcium release and simultaneously alleviates mitochondrial calcium overload in H9c2 cells following I/R injury. Furthermore, STIM2 knockdown decreases mitochondrial injury and preserves mitochondrial function following I/R injury. Collectively, these results suggest that the protective role of STIM2 knockdown against I/R injury in cardiomyocytes is associated with the reduced mitochondrial calcium overload and preserved mitochondrial function. Hence, our study may provide a novel insight into the regulation of mitochondrial-mediated cardiomyocyte apoptosis following I/R injury." @default.
• W2951236951 created "2019-06-27" @default.
• W2951236951 creator A5034600235 @default.
• W2951236951 creator A5063536264 @default.
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• W2951236951 date "2020-04-01" @default.
• W2951236951 modified "2023-10-02" @default.
• W2951236951 title "STIM2 knockdown protects against ischemia/reperfusion injury through reducing mitochondrial calcium overload and preserving mitochondrial function" @default.
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• W2951236951 doi "https://doi.org/10.1016/j.lfs.2019.116560" @default.
• W2951236951 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31200000" @default.
• W2951236951 hasPublicationYear "2020" @default.
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