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The inhibition of low-density lipoprotein cholesterol (LDL-C) oxidation refers to the prevention of chemical modification of LDL particles by reactive oxygen species (ROS) and other oxidants, a process that yields oxidized LDL (ox-LDL). Oxidized LDL plays a pivotal role in the initiation and progression of atherosclerosis by mediating foam cell formation, promoting endothelial dysfunction, and contributing to plaque instability and rupture. Therapies or interventions that inhibit this oxidation process are of interest for reducing cardiovascular risk, but "inhibition of LDL oxidation" is a goal achieved via modulation of several metabolic enzymes, antioxidants, and lifestyle interventions; it is not a single molecular target. This process is not a singular drug target but signifies the process or pathway by which interventions reduce the pathological oxidation of LDL, a critical event in atherogenesis.
Reducing reactive oxygen species (ROS) that drive LDL oxidation. Enhancing antioxidant enzyme activity (e.g., paraoxonase-1, LCAT). Directly scavenging free radicals that would otherwise oxidize LDL. Reducing small dense LDL particles that are more susceptible to oxidation (e.g., weight loss, statins). Inhibiting enzymes or pathways involved in LDL modification (e.g., Lp-PLA2 inhibitors).
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