RESUMEN
Objective: To investigate the role of miR-362-3p and its target in cardiomyocytes with hypoxia/reoxygenation (H/R) injury. Results: We found that miR-362-3p was decreased in myocardial infarction (MI) samples, and promoted the proliferation and restrained the apoptosis of H/R-injured H9c2 cells. TP53INP2 was recognized as the target of miR-362-3p and negatively modulated by miR-362-3p. Furthermore, the promotive effect of miR-362-3p on the proliferation of H/R-injured H9c2 cells was weakened by pcDNA3.1-TP53INP2, while the suppression on the apoptosis of H/R-injured H9c2 cells triggered by an miR-362-3p mimic was increased by pcDNA3.1-TP53INP2 by regulating apoptosis-associated proteins, as well as SDF-1 and CXCR4. Summary: miR-362-3p/TP53INP2 axis could ameliorate H/R-induced injury to cardiomyocytes by adjusting the SDF-1/CXCR4 signaling pathway.