Effect on MicroRNA-92a in Atherosclerosis along with FlowMediated Vasodilation Study

Abstract

Atherosclerosis has been regarded as an inflammatory disease. The vascular endothelium is considered as having multiple functions, regulating vascular tone, thrombosis, haematosis, permeability and cell adhesion. The emergence of microRNAs (miRNAs) as significant regulators of pathophysiological processes has indicated novel molecular insights and provided new therapeutic targets in atherosclerotic condition. Many studies have revealed that miRNA are associated with cardiovascular disease (CVD). With respect to miR-92a, miR -92a, a member of the miR-17 to miR-92 cluster, is expressed highly in endothelial cells (ECs) and regulated by shear stress. Both In vitro and vivo, miR-92a expression is highly induced in atheroprone regions compared with atheroresistant regions under disturbed flow (d-flow) condition. The clinical and experimental studies have suggested that inhibition of miR-92a can contribute to the improvement of endothelial dysfunction, inflammation, and oxidative stress in atherosclerosis. Recent reports showed that antimiR-92a as novel therapeutic options can be attributed to the endothelial cell autophagy and cardiomyocyte metabolism and that mechanistically, atherosclerotic status promote the packaging of functional miR-92a-3p into endothelial microvesicles, thereby promoting angiogenic response into recipient endothelial cells. It is strongly suggested that miR-92a-3p, having novel biological function and mechanism is a potent therapeutic target in atherosclerosis-related diseases. It is putative that flow-mediated vasodilation (FMD) study, early surrogate marker of endothelial function may in part reflect miR-92a, multifunctional biomarker