LAUSR

Myocardial ischemia/reperfusion (I/R) injury is a leading cause of morbidity and mortality. In this study, we investigated the role of miR‐192‐5p in hypoxia/reoxygenation (H/R)‐induced cardiomyocyte apoptosis. H9c2 cardiomyocytes were subjected to H/R and tested for miR‐192‐5p expression. Overexpression and knockdown experiments were performed to determine the effects of manipulating miR‐192‐5p on apoptotic responses. H/R‐treated H9c2 cells exhibited a 2.2‐fold increase in miR‐192‐5p levels. Overexpression of miR‐192‐5p significantly augmented apoptosis in H9c2 cells after H/R, which was accompanied by a significant increase in the ratio of Bax/Bcl‐2. In contrast, delivery of anti‐miR‐192‐5p inhibitors significantly reduced apoptosis induced by H/R. FABP3 was identified to be a functional target of miR‐192‐5p. Restoration of FABP3 prevented apoptosis in miR‐192‐5p‐transfected H9c2 cells, whereas downregulation of FABP3 enhanced apoptosis in H/R‐exposed H9c2 cells. In conclusion, miR‐192‐5p mediates H/R‐induced apoptosis in cardiomyocytes by targeting FABP3 and represents a potential target for prevention of myocardial I/R injury.