miR-125b-5p alleviates the damage of myocardial infarction by inhibiting the NFAT2 to reduce F2RL2 expression.

To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 ()/ on myocardial infarction (MI). After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of on the process of MI were observed, the effects of miR-125b-5p// on the cell viability, apoptosis, and inflammatory factors levels were determined. silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while silencing offset the effects of NFAT2 overexpression. MiR-125b-5p alleviates MI injury by inhibiting level to reduce expression.