[What is the role of Oxidised Low Density Lipoproteins in atherosclerotic vascular disease?]

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Abstract

The oxidation of low density lipoprotein (LDL) is considered a critical factor in atherogenesis. Theoxidation is the result of the balance between stimulating endogenous prooxidants and antioxidants present in LDL. This balance is strictly dependent on the concentration of oxidizable substrates that is to say, the unsaturated fatty acids. The central role of low density lipoprotein (LDL) in atherogenesis has been established for many years. However, no mechanism has direct atherogenic LDL could be attributed to the native state. This paradox has raised the hypothesis of changes in LDL increases their atherogenic potential, the foremost of which is oxidation. Initiating mechanisms in vivo peroxidation of LDL is still uncertain, but strong arguments supporting the existence of in vivo oxidized LDL in atherosclerotic lesions. Oxidized LDL is involved in all stages of the atherosclerotic reaction. This brief review summarizes the various mechanisms by which oxidized LDL promotes the progression of lesions. Some clinical studies have found a correlation between the title of autoantibodies to oxidized LDL and atherosclerosis, or between susceptibility to oxidation of LDL and the severity of the disease coron plow. These results need to be confirmed and extended. Observational studies have suggested a cardioprotective role of antioxidant vitamins. However, no intervention study has yet shown a possible effect of antioxidants on disease coronaraire. Such studies are urgently needed before a potential therapeutic anti-oxidant can be considered in the management of atherosclerosis.

Key words: Peroxidation, Oxidation, Lipoprotein LDL, Atherosclerosis, Pathogenesis, Antibody, Cardiovascular disease, vascular disease

Introduction

Oxidized LDL is well known factor that is critical in atherogenic mechanisms. OxLDL found in atheromatous lesions where they stimulate cholesterol esterification and OxLDL are degraded more rapidly by macrophages (Simons, 1986, 5-10). Atheromatous lesions are found in Stimulate where they are degraded by cholesterol esterification and macrophages more rapidly. The passage of native or modified LDL (like small LDL and dense LDL) to the subendothelium, their oxidation by reactive oxygen species, the liberation of cytoquines with chemiotactic properties, the migration of monocytes into the subendothelium promoted by adhesion molecules, the evolution of monocytes to macrophages and the internalization of LDLOX into foam cells are fundamental steps in the early deposition of cholesterol in the subendothelium (Stehbens, 1990, 119-136). The passage of native or modified LDL like small, dense LDL to the subendothelium, Their oxidation by reactive oxygen species, with the liberation of cytoquines chemiotactic properties, the migration of monocytes Into the subendothelium promoted by adhesion molecules, the evolution of monocytes to macrophages and Into the internalization ...