The Role of MicroRNAs, NO Synthases, Kinases, K<sub>ATP</sub> Channelsin the Infarction-Limiting Effect of Adaptation to Hypoxia
It has been established that chronic hypoxia (CH) significantly alters the expression of microRNAs in the myocardium. It was shown that miR-138 and miR-184 increase the tolerance of cardiomyocytes to hypoxia, while microRNA 199a 5p and miR-23b decrease the resistance of cardiomyocytes to hypoxia. CH enhanced expression of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS). It was shown the cardioprotective effect of CH is associated with the activation of iNOS. It was found that the infarction-limiting effect of chronic CH depends on mitoK<sub>ATP</sub> channel opening. It was established that the δ and ε isoforms of protein kinase C are involved in the cardioprotective effect of adaptation to hypoxia. Chronic hypoxia has been shown to increase expression of kinases: CaMKII, p-ERK1/2, p-p38, p-Akt, hexokinase-1, hexokinase-2. Hypoxia enhances the hexokinase-2 translocation to mitochondria. In animals adapted to hypoxia, it was not detected an increase in the expression of kinases: PKA, p-GSK3β, AMPK and JNK. Presented data are indicated that ERK1/2, MEK1/2 kinases are involved in the cardioprotective effect of adaptation to hypoxia. Myocardial hypertrophy caused by chronic hypoxia is associated with the activation of Rho kinase. The role of PI3K, Akt JNK, PKG, Rho kinase, mTOR, and p38 kinase in the protective effect of adaptation to hypoxia is controversial. The purpose of the review: analysis of data on the role of miRNAs, NO synthase, and kinases in the cardioprotective effect of CH.