Genetic Polymorphisms of Inflammatory Mediators in Atherosclerosis

In the vascular wall of large arteries, cellular and humoral immune responses are elicited as a consequence of diverse noxious stimuli within subendothelial space, which further derives in endothelial dysfunction, the accumulation of lipids and formation of the atheromatous plaque. Monocytes, macrophages, T cells, endothelial cells and smooth muscular cells are all players in this inflammatory-atherosclerotic process, which is not only genetically regulated but also influenced by environmental factors. In this review, the summary of genetic variants in major immune mediators associated with the evolution of atherosclerosis is presented.