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Figure 1 Role of cholesteryl ester transfer protein (CETP) in plasma lipid transport. Cholesteryl ester transfer protein promotes bidirectional transfers (shown by the red arrows) of cholesteryl esters (CE) and triglycerides (TG) between high-density lipoproteins (HDLs), very low-density lipoproteins (VLDLs), and low-density lipoproteins (LDLs). Most of the CEs in plasma originate in HDLs in a reaction catalyzed by lecithin:cholesterol acyltransferase (LCAT), while the majority of the TG enters plasma as a component of TG-rich lipoproteins secreted either from the liver as VLDLs or from the intestine as chylomicrons. Very low-density lipoproteins are subsequently converted into LDLs after hydrolysis of a proportion of their TG by lipoprotein lipase (LPL) and hepatic lipase (HL). The overall effect of the CETP-mediated CE exchanges between these lipoproteins is a net mass transfer of CE from the antiatherogenic HDLs to the potentially proatherogenic VLDLs and LDLs. The cholesterol in LDLs is taken up by all cells (both in liver and peripheral tissues) that express the LDL receptor. Modified (oxidized) LDLs are also taken up by macrophages in a scavenger receptor-mediated process that converts the macrophage into a foam cell. Cholesterol, both in its free or unesterified form (FC) and in its esterified form as CE, is returned to the liver by HDLs via the scavenger receptor-B1 (SR-B1) (pathway 1) and by LDLs via the LDL receptor (LDL-R) (pathway 2). See Figure 2 for mechanisms through which peripheral cells may efflux cholesterol to HDL particles.