[Modern view on biochemistry of atherosclerosis]

The article summarizes the literature data on clinical chemistry of pathogenesis of atherosclerosis. According to the up-to-date view, atherogenic are considered the products of chemical modification of LDL, rather than LDL themselves. The modification is created by means of the free radicals or reactive oxidised nitrogen species (RONS). Their rapid and uncontrollable generation in the body may become a prerequisite for the development of a number of diseases and pathological processes, such as atherosclerosis, neurological, malignancies, aging and inflammation and etc... The article describes the chemical nature of free radicals, the mechanism of their action and chain character of their generation. The particular attention is paid to nitric oxide, which is recognized in a broad array of biologic systems, namely, actions on vascular endothelium and mediating macrophage activity. The mechanisms of cell protection from the toxic action of RONS have been elucidated. Based on the experimental data presented, extremely large doses of antioxidants may lead to health problems, rather than confer benefits, because RONS are involved in the mechanisms which increase the survival of cells at unfavourable conditions. The complete impairment of their generation promotes the weakening of cell immunity. The article describes the means to provide cellular cholesterol homeostasis and the uptake of chemically modified LDL by macrophage scavenger receptors. Macrophages consume excess modified lipoprotein becoming foam cells. Foam cells accumulate, releasing growth factors and cytokines that stimulate the migration of smooth muscle cells from the media to the intima, where they proliferate, produce collagen and take up lipid, potentially becoming foam cells which are the main culprits of atherosclerotic changes in the artery walls.