**2. Atherosclerosis and restenosis**

Vascular cell activation and remodeling are the principle events in vascular pathologies such as atherosclerosis, transplant vasculopathy, post angioplasty restenosis, in-stent restenosis and bypass graft failure [33, 34]. It is realized that injury to vessel wall by various atherogenic insults sets-off inflammatory response causing endothelial cell dysfunction. Following endothelial cell dysfunction, VSMC in the media that are quiescent and contractile in nature, migrate to intima in response to local inflammation and become proliferative cells. VSMC are highly specialized cells whose principal function is to regulate the attributes of blood vessels in the body by appropriately responding to changes in the volume of blood vessels and the local blood pressure to facilitate distribution of oxygenated blood to different parts of the body. In adult vessels, VSMC proliferate at very low rate; display reduced synthetic activity; and express a unique compilation of proteins that is characteristic of contractile phenotype such as contractile proteins, ion channels, and signaling molecules. Yet, they still maintain remarkable plasticity and retain the ability to undergo extreme and reversible changes in phenotype in response to their local environmental signals, especially during vascular development, and in response to vascular injury as a key mechanism in wound healing. It is recognized vascular injury provoked by various atherogenic insults such as mechanical, chemical and immuno‐ logical injuries triggered by different disease risk factors promote VSMC activation, migration and proliferation, which are precursors to the development of atherosclerosis and neointimal hyperplasia [34, 35]. VSMC also undergo phenotypic modification from contractile to prolif‐ erative or synthetic phenotype in conjunction with vessel remodeling by altering the cell number and composition of vessel wall as the primary pathophysiological mechanism in different clinical pathologies such as postangioplasty restenosis, in-stent restenosis, and vein bypass graft failure and transplant vasculopathy [34-37]. However, the molecular mechanisms involved in VSMC phenotypic control are still vague.

During the last few years there is an upsurge in ncRNA research specifically pertaining to a novel class of small miRNAs because of their role in various biological functions. In a variety of eukaryotic organisms miRNAs have been demonstrated to play key roles in various cellular processes including proliferation, differentiation, and apoptosis [38-40], which are central to normal development and physiology, and pathogenesis of diseases. As such, dysregulation of miRNAs has been linked to different diseases, including different cancers, neurological, cardiovascular and other diseases [22, 25-32]. Because of their effects on cellular processes as gene expression regulators, impairment of miRNAs as evidenced in many cancers, suggest involvement of miRNAs in the phenotypic modulation of VSMC both in normal and disease states. Here we briefly describe miRNAs, their biogenesis and mechanism of action and then summarize the recent progress in the functional significance of miRNAs in VSMC phenotypic modulation and response to injury.
