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Oxidized low-density lipoprotein (oxLDL) is a chemically modified form of LDL that results from the oxidative transformation of its lipid and protein components (primarily apolipoprotein B-100) by reactive oxygen species or enzymes like myeloperoxidase and lipoxygenases [11, 12]. It is a critical driver in the initiation and progression of atherosclerosis, as it is not recognized by the standard LDL receptor but is instead taken up rapidly by scavenger receptors, notably the lectin-like oxidized LDL receptor-1 (LOX-1) [1, 15]. This uptake by macrophages leads to the formation of foam cells, the hallmark of atherosclerotic plaques, and triggers a cascade of pro-inflammatory, pro-thrombotic, and pro-apoptotic signaling in the vascular wall [2, 10, 17].\n\nTherapeutic strategies aim to either prevent the oxidation of LDL or neutralize the effects of the oxidized particle. Classical approaches involve antioxidants like probucol and succinobucol, which inhibit the lipid peroxidation process, or the use of statins and PCSK9 inhibitors to reduce the total pool of LDL available for oxidation [3, 7, 13]. More targeted emerging therapies involve monoclonal antibodies that block the interaction between oxLDL and its receptors, such as LOX-1, to mitigate vascular inflammation and plaque instability [5, 21]. Circulating levels of oxLDL are used as potent biomarkers for identifying patients at high risk of cardiovascular events, often providing better predictive value than standard lipid profiles [4, 8].
Antioxidant-mediated inhibition of lipid peroxidation; Competitive inhibition of scavenger receptor binding; Reduction of native LDL substrate available for oxidation.
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