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Needed: a better understanding of the antiatherogenic properties of HDL.

DOI:10.1097/MOL.0b013e3283654ee6 A number of studies in large populations have supported an inverse risk association of HDL cholesterol (HDL-C) with coronary disease. Several studies involving increases in HDL-C induced by inhibition of cholesteryl ester transfer protein have not demonstrated benefit. Failure to detect benefit from niacin treatment may reflect inappropriate study design, in view of positive outcomes in past studies and in a patient subset in a recent trial. Understanding the antiatherogenic properties of HDL will depend on much deeper appreciation of its molecular heterogeneity and the numerous associated activities that may confer protection [1]. Many molecular species of HDL are lost during ultracentrifugal separation, but selected affinity immunosorption reveals over 20 discrete entities. Mass spectrometry yields nearly 100 protein species [2 && ], revealing differences between normal HDL and that of patients with coronary disease, including proteins proapoptotic for endothelium [3 & ] and a group of protease inhibitors that may protect the arteries against leukocyte-mediated proteolysis. The lipidome of HDL is now under study, revealing many phospholipid species [4 && ], among them sphingosine-1-phosphate (S1P), which is bound to apolipoprotein M [5], activating nitric oxide synthase and kinase Akt in vascular endothelium [6 & ]. It is likely that other quantitatively minor lipid species will have discrete metabolic or regulatory roles. HDL molecular species can affect local concentrations of amphipathic lipids that confer special properties on domains of cell membranes (lipid rafts) that facilitate transport activities such as cholesterol efflux, and other critical functions such as immune cell activation [7]. The lipid and protein contents of HDL are influenced by abnormalities in other lipoproteins. The cholesteryl ester content is dependent on the level of triglyceride-rich lipoproteins that provide the thermodynamic sink for cholesteryl ester transfer. With high triglycerides, smaller HDL particles prevail, including a higher level of prebeta-1 HDL. A newly emerging potential for metabolic regulation comes with the discovery