High-density lipoproteins and cardiovascular disease: 2010 update

Abstract

High-density lipoprotein-cholesterol (HDL-C) is a continuous inverse cardiovascular risk factor. The mechanisms by which HDLs protect against atherosclerosis are multiple. The major effect is thought to be reverse cholesterol transport, the mechanism by which excess cellular cholesterol is returned to the liver for excretion in the bile. HDLs also have pleiotropic roles: they decrease inflammation, prevent low-density lipoprotein oxidation, vascular endothelial cell apoptosis and thrombosis, and improve vascular endothelial function. Recent studies suggest that nascent HDL particles are metabolized rapidly and that their components (Apo AI, cholesterol and phospholipids) are rapidly exchanged within lipoprotein classes. There are many causes of HDL-C deficiency. Using Mendelian randomization, several groups have concluded that many genetic forms of HDL deficiency do not increase cardiovascular risk. This raises the controversial issue of the causality of low HDL-C as a cardiovascular risk factor, rather than a marker of cardiovascular health. This is reflected in the importance of lifestyle in determining HDL-C levels. The treatment of low HDL-C remains controversial, in part because the only currently available effective medication, niacin, is relatively poorly tolerated and outcomes studies on cardiovascular disease prevention are still pending.

Serum amyloid A impairs the antiinflammatory properties of HDL

“…Because HDL-cholesterol levels can drop following acute inflammatory stimuli (6), it has been suggested that low HDL cholesterol levels associated with obesity are a result of chronic, low-grade inflammation (6). HDL has several functions, including mediation of reverse cholesterol transport (7) and inhibition of inflammation (8)(9)(10)(11), oxidation (12,13), and endothelial activation (14,15).…”

HDL-Related Mechanisms of Olive Oil Protection in Cardiovascular Disease

“…Furthermore, the use of image techniques in epidemiological studies has shown that the atherosclerotic plaque progression in individuals with carotid estenosis was smaller in those that presented high levels of HDL-C [28]. Current knowledge is still, however, insufficient to recommend desirable levels [29,30].…”

“…In the arterial wall, the removal C from macrophages by HDL may prevent its accumulation and transformation into foam cell, and thereby atherosclerosis [30,45]. The first stage of the reverse transport is the C efflux from the cells to the fraction pre-1 of the HDL, initiated by ABCA1-mediated C transport to lipid-poor APOA1.…”

“…Other aspects of HDL include: 1) anti-inflammatory properties (diminishing the cellular and humoral mediators of the arterial inflammation) which are attributed to their sphingosine-1-phosphate content [52,53]; 2) antithrombotic/ profibrinolytic effects (reducing platelet aggregation and coagulation); 3) vasorelaxation effects (increasing the production of prostacyclin and nitric oxide); 4) proliferation and migration of the endothelial cells; and 5) apoptosis inhibition of the endothelial cells [30,45,48,54]. Anti-inflammatory Sphingosine-1-phosphate [52,53] Antithrombotic/profibrinolitic Reducing Platelet Aggregation and Coagulation [30,45,48,54] Vasorelaxation Increasing the Production of Prostacyclin and Nitric Oxide [30,45,48,54] Proliferation and migration of the endothelial cells [30,45,48,54] The present review addresses the current available information regarding the effect of OO on HDL in humans and in different animal models.…”

“…Anti-inflammatory Sphingosine-1-phosphate [52,53] Antithrombotic/profibrinolitic Reducing Platelet Aggregation and Coagulation [30,45,48,54] Vasorelaxation Increasing the Production of Prostacyclin and Nitric Oxide [30,45,48,54] Proliferation and migration of the endothelial cells [30,45,48,54] The present review addresses the current available information regarding the effect of OO on HDL in humans and in different animal models.…”