Assessing low levels of high-density lipoprotein cholesterol as a risk factor in coronary heart disease
A working group report and update
Antonio M. Gotto, Jr, MD, DPhil*,* and
Eliot A. Brinton, MD
* Weill Medical College of Cornell University, New York, New York, USA
University of Utah School of Medicine, Salt Lake City, Utah, USA
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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.
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