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Emerging roles of qualitative properties of lipoproteins in atherosclerosis.

DOI:10.1097/MOL.0000000000000119 miologic research on the relationship of lipoproteins with arteriosclerotic disease has treated lipoproteins as homogeneous entities. Most studies have been restricted to measurement of the cholesterol or triglyceride contents of lipoproteins separated by ultracentrifugation or differential precipitation. A more molecular view is emerging that strongly supports the concept that important differences can exist among the classical lipoprotein species, independent of their levels. These can involve changes in the species distribution of lipids, especially the inclusion of oxidatively modified lipids, and the extensive covalent alteration of protein constituents. It is already appreciated that both of these have significant impacts on the antiatherogenic properties of native lipoproteins. Further qualitative differences involve the acquisition of apolipoprotein J (clusterin) and serum amyloid associated proteins as a result of inflammation, and, possibly, changes in the burden of microRNA in HDL [1 & ]. It is likely that structural alterations in lipids and proteins in lipoproteins underlie impairment of antiatherogenic activity, such as the diminished anti-inflammatory activity of HDL associated with myocardial infarction [2 && ]. Alteration of the lipid constituents of lipoproteins: Covalent modification of lipids in lipoproteins is caused both by lipoxygenases and by reactive oxygen species. The latter arise from myeloperoxidase, NADPH oxidase, or xanthine oxidase, all of which mediate the formation of peroxyl radicals [3 && ]. A previously unknown class of covalently altered lipids, N-modified phospholipids, are now known to be generated from other oxidized lipid species and increase the activity of plateletactivating factor and thrombin activity [3 && ]. The identification of covalently modified lipids in atheromata suggests that they are quantitatively important in atherogenesis [4 & ]. It is clear that there is a significant alteration in the lipid composition of HDL in individuals with diabetes and cardiovascular disease [5], and even in heart failure [6 & ]. It is likely that the formation of Schiff base adducts on apolipoproteins by aldehydic lipids formed by oxidation impairs their function and leads to neoantigen formation. Sphingosine-1-phosphate carried in HDL,