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Abstract
Genetic, clinical, and pharmacological studies implicate elevated levels of LDL in the pathogenesis of atherosclerotic vascular disease, the leading cause of death in industrialized societies (1). Paradoxically, native LDL fails to exert potentially atherogenic effects in vitro, suggesting that it must be modified to promote vascular disease. Indeed, many lines of evidence support the LDL oxidation hypothesis, which suggests that oxidative damage to LDL is one important mechanism for rendering lipoproteins atherogenic (as reviewed in Refs. 2, 3).
Highlights
Genetic, clinical, and pharmacological studies implicate elevated levels of LDL in the pathogenesis of atherosclerotic vascular disease, the leading cause of death in industrialized societies [1]
The strong relationship between low levels of HDL and the risk for atherosclerosis and coronary artery disease (CAD) has been attributed to several distinct mechanisms
Lipid hydroperoxides are the initial products when lipids are damaged by 1-electron oxidants, such as tyrosyl radical and nitrogen dioxide radical
Summary
Clinical, and pharmacological studies implicate elevated levels of LDL in the pathogenesis of atherosclerotic vascular disease, the leading cause of death in industrialized societies [1]. Enzymes carried by HDL, including paraoxonase-1 (PON-1), LCAT, and lipoprotein-associated phospholipase A2, have been proposed to degrade lipid oxidation products [12,13,14]. These observations suggest that HDL might play major roles in the transport and metabolism of lipid hydroperoxides in vivo and that these processes contribute to its cardioprotective effects.
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