[Molecular Mechanism and Evaluation Method for Anti-Inflammatory HDL]

Plasma concentrations of high-density lipoprotein cholesterol (HDL-C) are inversely correlated with the risk of coronary artery disease (CAD). The cardioprotective effect of HDL is attributable to its reverse cholesterol transport capacity from peripheral cells to the liver. HDL has a variety of anti-inflammatory, anti-oxidative, and anti-apoptotic properties. However, recent interventional therapies using CETP inhibitors or niacin did not prove to be of benefit in the reduction of cardiovascular risks. This discrepancy is often explained by the quality of HDL particles. HDL particles undergo oxidation, chloralization, nitration, and calbamilation, under conditions due to inflammatory or metabolic disorders. HDL particles with these modifications may lose their atheroprotective effects and promote inflammatory processes, being referred to as dysfunctional HDL. HDL consists of a variety of phospholipids and proteins such as apolipoprotein A-I and paraoxonase-1. Because these components in the HDL particle regulate anti-atherosclerotic effects, the significance of HDL should be evaluated based on the HDL function. Reliable assays and surrogate markers of HDL function will be useful for evaluating the efficacy of HDL-targeted interventions against atherosclerosis. In this review, we summarized the mechanism of anti-inflammatory effects on HDL and assays for evaluating HDL functions.