ABSTRACT
During the past three decades, there has been continuing evidence indicating that lipid oxidation plays a key role in atherosclerosis and cardiovascular diseases. Oxidized phospholipids rise from oxidation of low-density lipoprotein (LDL) phospholipids that contain arachidonic acid. These molecules are recognized by the innate immune system in humans and in animal models. Lipoxygenase and myeloperoxidase pathways generate these oxylipids, and antioxidants including vitamin E are not able to prevent their formation, partially explaining the failure of antioxidant vitamins to inuence clinical outcomes. High-density lipoprotein (HDL) is capable of preventing lipid oxidation in many settings. The main function of HDL has been suggested to be reverse cholesterol transport (RCT), and now the oxidation hypothesis of atherogenesis and RCT seem to have common biological relations and basis. While normal HDL is capable of preventing oxidative modication of lipids and thus serving as an anti-inammatory molecule, HDL from patients with atherosclerosis, heart failure, diabetes, obesity, lupus, Crohn’s disease, HIV infection, renal failure, and other metabolic disorders is dysfunctional and not capable of preventing lipid oxidation.
