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Lipid peroxidation in low-density lipoprotein (LDL) particles is a process wherein free radicals and other reactive oxygen species oxidize polyunsaturated fatty acids and cholesterol esters within LDL, as well as their associated apolipoprotein components, notably ApoB100. This oxidative modification transforms native LDL into oxidized LDL (Ox-LDL), which is rapidly taken up by macrophages through scavenger receptors, initiating foam cell formation and arterial plaque build-up. Ox-LDL strongly promotes inflammatory and immune responses, endothelial dysfunction, smooth muscle cell migration and proliferation, all central features in the development and progression of atherosclerosis. Interventions focus on reducing LDL levels, scavenging oxidative species, increasing antioxidant intake, or directly neutralizing Ox-LDL, all with the aim of minimizing cardiovascular risk. Circulating levels of oxidized LDL serve as biomarkers for risk assessment and efficacy monitoring, but clinical application is limited by measurement challenges and lack of standardization.
Reduction of LDL cholesterol levels (decreasing substrate for oxidation) Enhancement of antioxidant defenses (reducing formation of oxidized LDL) Direct scavenging of free radicals Blocking Ox-LDL receptors on vascular cells (e.g., via experimental antibodies)
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