MiR-137-3p exacerbates the ischemia-reperfusion injured cardiomyocyte apoptosis by targeting KLF15.

Ischemia-reperfusion (I/R) injury is a kind of the tissue damage caused by an abrupt re-supplying tissue with blood after a period of ischemia or hypoxia. It contributes to a wide range of pathological processes including kidney injury, circulatory arrest, and especially cardiovascular disease. However, the underlying pathological mechanism is not fully elucidated. Previously, extensive studies demonstrated that miRNAs participate in the pathogenesis of I/R injury, such as I/R-induced cardiomyocyte apoptosis. Here, we found that miR-137-3p, a mature form of miR-137, was up-regulated in I/R-injured cardiomyocytes of myocardial infarction patients. Deficiency of miR-137-3p partly alleviated the cardiomyocyte apoptosis and oxidative stress induced by hypoxia-reoxygenation (H/R) treatment in H9c2 cells. Also, we provided evidences that miR-137-3p directly targeted the 3' UTR of KLF15 mRNA to down-regulate its expression, and loss function of KLF15 significantly abolished the deleterious effects of ectopic miR-137-3p on cardiomyocytes both in vitro and in vivo. Collectively, these observations highlight a molecular perturbation in the pathogenesis of I/R injury in cardiomyocytes.