Reduction of miR-29a-3p induced cardiac ischemia reperfusion injury in mice via targeting Bax

The current study mainly aimed to evaluate the expression and the potential mechanism of miR‑29a‑3p in the hearts of mice after cardiac ischemia reperfusion (CIR) injury. Quantitative PCR was carried out to assess the relative levels of miR‑29a‑3p in the hearts of a CIR injury mouse model. To the best of our knowledge, the current study is the first to show that the level of miR‑29a‑3p was significantly decreased in the hearts of CIR injury mouse models compared with that of sham controls. Moreover, the authors found that decreased miR‑29a‑3p levels enhanced the production of reactive oxygen species in cardiomyocytes. Meanwhile, the inhibition of miR‑29a‑3p induced substantial cardiomyocyte apoptosis. Further study showed that the inhibition of miR‑29a‑3p decreased the activation of Akt and p38, suggesting a stress‑induced self‑regulatory mechanism after CIR injury in primary cardiomyocytes. A dual luciferase assay and western blot analysis showed that Bax was a target gene of miR‑29a‑3p. The authors also measured the level of miR‑29a‑3p in the plasma of 100 acute myocardial infarction (AMI) patients and found that circulating miR‑29a‑3p was significantly decreased in AMI patients. Receiver operating characteristic curve analysis showed that miR‑29a‑3p could be used to screen AMI patients from healthy controls. Hence, the authors of the current study propose that reduced miR‑29a‑3p levels in primary cardiomyocytes contribute to CIR injury‑related apoptosis mainly by targeting Bax.