It also damage thw endothelial cells by preventing the synthesis of endogenous relaxing factors, as well as increasing the expressions of monocyte chemotactic protein-1 and interleukin-8 in endothelial cells through the activation of the NADH/NADPH oxidase system, which can lead to atherosclerosis and inflammatory diseases28,29. This evidence concerns the gene CCL2 and atherosclerosis.