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Figure 1 This figure illustrates reverse cholesterol transport, which delivers cholesterol from peripheral cells to the liver for excretion in the bile. The adenosine triphosphate binding cassette (ABC)-A1 transporter mediates the efflux of free cholesterol from peripheral cells, notably macrophages, to apolipoprotein (apo) A-I–rich nascent high-density lipoprotein (HDL). Esterification by lecithin:cholesterol acyltransferase (LCAT) results in the formation of mature spherical HDL₂ particles. Following cholesteryl ester transfer protein (CETP)-mediated exchange of cholesteryl esters (CE) for triglycerides, the latter are hydrolyzed by hepatic lipase (HL). The CE still associated with HDL₂ are then selectively removed from plasma by the scavenger receptor B1 (SR-B1) in the liver ("direct" reverse cholesterol transport [RCT]), resulting in small, lipid-poor apo A-I particles (senescent HDL) that are susceptible to glomerular filtration and endocytosis by the cubilin/megalin receptors in the renal proximal tubule. A portion of the CE transferred to apo-B–containing particles (very low-density lipoprotein [VLDL], intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL]) are transported to the liver for uptake by the LDL receptor ("indirect" RCT). Courtesy of Craig T. Basson, MD, PhD, and Carl J. Vaughan, MD, MRCPI. Reprinted with permission. LDL-R = low-density lipoprotein receptor; LPL = lipoprotein lipase; mLDL = modified low-density lipoprotein.