Pharmacologic augmentation of high-density lipoproteins: mechanisms of currently available amd emerging therapies

Purpose of review With the limited effects of low-density lipoprotein-based lipid intervention, more attention is being paid to drugs that augment or mimic high-density lipoprotein's beneficial effects. A thorough understanding of the anti-atherogenic effects of high-density lipoprotein, and the mechanisms of existing or emerging high-density lipoprotein-based therapies, is essential for rational strategy for the prevention of cardiovascular disease. Recent findings High-density lipoprotein mediates its beneficial effects through reverse cholesterol transport and direct anti-inflammatory effects of apolipoprotein Al and other component parts. Currently available drugs increase high-density lipoprotein-C through increasing apoAl synthesis (statins, fibrates) and decreasing apolipoprotein Al catabolism (niacin). Cholesteryl ester transfer protein inhibitors dramatically raise high-density lipoprotein-C, but clinical data are still required to verify their cardio protective effects. Novel therapies such as apolipoprotein Almilano, apolipoprotein Al mimetic peptide, and exogenous phospholipids show tremendous promise as treatments for atherosclerosis. Summary High-density lipoprotein and its defining functional protein apoAl prevent atherosclerosis through reverse cholesterol transport and other direct effects. Research has led to the development of novel therapies that increase high-density lipoprotein-C or that mimic direct anti-atherogenic effects of apolipoprotein Al. As these emerging therapies find a place in clinical medicine, we can anticipate preventing a much higher degree of cardiovascular events.