Genetic and Epigenetic study in progression of atherosclerosis

Abstract

Atherosclerosis is a chronic disease of large and medium sized arteries which is characterized by accumulation of cholesterol in the arterial wall together with proliferation of arterial smooth muscle cells and accumulation of extracellular matrix components which lead to occlusion of blood vessels, myocardial infarction, peripheral vascular disease, amputations, aneurysms and stroke. Chronic inflammatory response with infiltration of monocyte–macrophages and T-cells and endothelial dysfunction are also prominent features of atherogenesis.
Atherosclerosis is a complex multifocal arterial disease involving interactions of multiple genetic and environmental factors. Advances in techniques of molecular genetics have revealed that genetic polymorphisms significantly influence susceptibility to atherosclerotic vascular diseases. A large number of candidate genes, genetic polymorphisms and susceptibility loci associated with atherosclerotic diseases have been identified in recent years and their number is rapidly increasing. The contribution of epigenetic mechanisms to cardiovascular diseases remains poorly understood. It remains unclear whether epigenetic changes are causally related to the pathogenetic features, such as clonal proliferation of lesion smooth muscle cells, lipid accumulation and modulation of immune responses in the lesions, or whether they merely represent a consequence of the ongoing pathological process. However, genetic and epigenetic changes could at least partly explain poorly understood environmental and dietary effects on atherogenesis and the rapid increases and decreases in the incidence of coronary heart disease observed in various populations