Oxidized LDL

LDL in its oxidized form, or oxLDL, is now generally acknowledged to be highly proatherogenic and to play a significant role in atherosclerotic plaque formation. ^[1] Oxidized LDL plays a more important role in the genesis and progression of atherosclerosis than native LDL. ^[2] Among the different atherogenic modifications of LDL within the vascular wall, oxidation represents a primary modification. ^[3]

Accumulation of oxidized LDL in the tunica intima triggers the onset of atherosclerosis, and the resulting plaques may later rupture, causing thrombosis and events such as myocardial infarction and stroke. ^[4] Oxidized LDL leads to endothelial dysfunction, expression of adhesion molecules and recruitment of monocytes into the subendothelial space, and is then taken up by macrophages via scavenger receptors such as LOX-1 to form foam cells. ^{[2] [3]} Oxidized LDL also acts as a sterile trigger of inflammation and thromboinflammation, contributing to thrombotic events beyond the arterial plaque. ^[5] Oxidized LDL is a product of oxidative stress in the vascular wall, where lipid and protein oxidation modify LDL in an early event of atherogenesis that drives foam cell formation and endothelial dysfunction ^[6]. The atherogenicity of oxidized LDL is mediated in part through the formation of HNE-apoB adducts, which redirect LDL metabolism toward the macrophage scavenger receptor pathway and foam cell formation ^[7]. Oxidized LDL is a modified form of native LDL cholesterol that plays a more important role in the genesis and progression of atherosclerosis than the unmodified particle ^[2].