Oxidized low-density lipoprotein (Ox-LDL) plays a critical role in atherogenesis. Hypercholesterolemia increases atherosclerosis risk, but the mechanisms linking it to atherogenesis remain unclear. Ox-LDL is modified by oxidation, which enhances its uptake by macrophages, leading to cholesterol accumulation and foam cell formation. Ox-LDL also exhibits chemotactic activity for monocytes, cytotoxicity, and the ability to alter gene expression in neighboring cells. It can induce the production of chemotactic factors like MCP-1, which recruit more monocytes to the site of atherosclerosis. Ox-LDL can also trigger immune responses, promote coagulation, and alter vasomotor properties of coronary arteries. Additionally, Ox-LDL may inhibit endothelial-dependent vasodilation by disrupting endothelial membranes and affecting nitric oxide production. Ox-LDL is formed through oxidation by endothelial cells, smooth muscle cells, or macrophages, or by exposure to copper ions. Oxidation involves lipid peroxidation and fragmentation, leading to the formation of reactive intermediates that modify apo B. These modifications alter LDL's recognition by the LDL receptor, reducing its uptake by macrophages. Ox-LDL can also be recognized by scavenger receptors, leading to its uptake and further modification. The variability in Ox-LDL preparation and oxidation stages can affect its biological activity and the interpretation of experimental results. Factors influencing LDL oxidation in vivo include the fatty acid composition of LDL, the antioxidant content, and the activity of enzymes like 15-lipoxygenase. Dietary modifications, such as reducing unsaturated fatty acids and increasing monounsaturated fatty acids, can reduce LDL susceptibility to oxidation. Antioxidants like probucol and vitamin E can protect LDL from oxidation and reduce atherosclerosis. However, the exact mechanisms by which Ox-LDL contributes to atherogenesis are still under investigation. The role of Ox-LDL in atherogenesis is complex, involving multiple pathways, including lipid accumulation, immune responses, and vascular dysfunction. Understanding these mechanisms is crucial for developing effective strategies to prevent and treat atherosclerosis. Current research focuses on identifying the factors that influence Ox-LDL formation and its biological effects, as well as exploring potential therapeutic interventions to inhibit LDL oxidation and reduce atherosclerosis risk.Oxidized low-density lipoprotein (Ox-LDL) plays a critical role in atherogenesis. Hypercholesterolemia increases atherosclerosis risk, but the mechanisms linking it to atherogenesis remain unclear. Ox-LDL is modified by oxidation, which enhances its uptake by macrophages, leading to cholesterol accumulation and foam cell formation. Ox-LDL also exhibits chemotactic activity for monocytes, cytotoxicity, and the ability to alter gene expression in neighboring cells. It can induce the production of chemotactic factors like MCP-1, which recruit more monocytes to the site of atherosclerosis. Ox-LDL can also trigger immune responses, promote coagulation, and alter vasomotor properties of coronary arteries. Additionally, Ox-LDL may inhibit endothelial-dependent vasodilation by disrupting endothelial membranes and affecting nitric oxide production. Ox-LDL is formed through oxidation by endothelial cells, smooth muscle cells, or macrophages, or by exposure to copper ions. Oxidation involves lipid peroxidation and fragmentation, leading to the formation of reactive intermediates that modify apo B. These modifications alter LDL's recognition by the LDL receptor, reducing its uptake by macrophages. Ox-LDL can also be recognized by scavenger receptors, leading to its uptake and further modification. The variability in Ox-LDL preparation and oxidation stages can affect its biological activity and the interpretation of experimental results. Factors influencing LDL oxidation in vivo include the fatty acid composition of LDL, the antioxidant content, and the activity of enzymes like 15-lipoxygenase. Dietary modifications, such as reducing unsaturated fatty acids and increasing monounsaturated fatty acids, can reduce LDL susceptibility to oxidation. Antioxidants like probucol and vitamin E can protect LDL from oxidation and reduce atherosclerosis. However, the exact mechanisms by which Ox-LDL contributes to atherogenesis are still under investigation. The role of Ox-LDL in atherogenesis is complex, involving multiple pathways, including lipid accumulation, immune responses, and vascular dysfunction. Understanding these mechanisms is crucial for developing effective strategies to prevent and treat atherosclerosis. Current research focuses on identifying the factors that influence Ox-LDL formation and its biological effects, as well as exploring potential therapeutic interventions to inhibit LDL oxidation and reduce atherosclerosis risk.