Dysfunctional High-Density Lipoprotein: An Innovative Target for Proteomics and Lipidomics

Figure 1

HDL metabolism and main components implicated in their antiatherogenic-anti-inflammatory functions. HDL metabolism consists of 3 phases. (a) Synthesis occurs in the liver and intestine, originating discoid or pre-β HDL. This subpopulation initiates RCT in peripheral tissues, mediated by Apo A-I binding to ABCA-1 and LCAT, resulting in HDL rich in cholesteryl esters. (b) HDL₃ are the first to form, which continue cholesterol capture in various tissues. Likewise, CETP transfers TAG to HDL, whereas PLTP mediates transfer of phospholipids and free cholesterol, increasing the size of the particles, yielding HDL₂. (c) Finally, HDL undergos exclusion through SR-B1 in hepatocytes, for either biliary secretion or formation of new lipoproteins. FC: free cholesterol; PL: phospholipids; ABCA-1: ATP-binding cassette transporter A-1; LCAT: Lecithin-Cholesterol Acyltransferase; PON: Paraoxonase; CETP: cholesteryl ester transfer protein; HL: hepatic lipase; EL: endothelial lipase; HDL: High-Density Lipoprotein; SR-B1: Scavenger Receptor B1.