Circulation Research. 2005;96:1221-1232
doi: 10.1161/01.RES.0000170946.56981.5c
doi: 10.1161/01.RES.0000170946.56981.5c
© 2005 American Heart Association, Inc.
Review |
New Insights Into the Regulation of HDL Metabolism and Reverse Cholesterol Transport
From the Departments of Medicine and Physiology (G.F.L), University of Toronto, Canada; The Institute for Translational Medicine and Therapeutics (D.J.R.), The Cardiovascular Institute, and the Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia.
Correspondence to Dr Gary Lewis, Toronto General Hospital, 200 Elizabeth St, Room EN11-229, Toronto, Ontario, M5G 2C4, Canada. E-mail gary.lewis{at}uhn.on.ca
This Review is part of a thematic series on New Pathways in HDL Metabolism, which includes the following articles:
Antiinflammatory Properties of HDL
Genetics of Variation in HDL Cholesterol in Humans and Mice
New Insights Into the Regulation of HDL Metabolism and Reverse Cholesterol Transport
Endothelial and Antithrombotic Effects of HDL
Daniel Rader Guest Editor
The metabolism of high-density lipoproteins (HDL), which are inversely related to risk of atherosclerotic cardiovascular disease, involves a complex interplay of factors regulating HDL synthesis, intravascular remodeling, and catabolism. The individual lipid and apolipoprotein components of HDL are mostly assembled after secretion, are frequently exchanged with or transferred to other lipoproteins, are actively remodeled within the plasma compartment, and are often cleared separately from one another. HDL is believed to play a key role in the process of reverse cholesterol transport (RCT), in which it promotes the efflux of excess cholesterol from peripheral tissues and returns it to the liver for biliary excretion. This review will emphasize 3 major evolving themes regarding HDL metabolism and RCT. The first theme is that HDL is a universal plasma acceptor lipoprotein for cholesterol efflux from not only peripheral tissues but also hepatocytes, which are a major source of cholesterol efflux to HDL. Furthermore, although efflux of cholesterol from macrophages represents only a tiny fraction of overall cellular cholesterol efflux, it is the most important with regard to atherosclerosis, suggesting that it be specifically termed macrophage RCT. The second theme is the critical role that intravascular remodeling of HDL by lipid transfer factors, lipases, cell surface receptors, and non-HDL lipoproteins play in determining the ultimate metabolic fate of HDL and plasma HDL-c concentrations. The third theme is the growing appreciation that insulin resistance underlies the majority of cases of low HDL-c in humans and the mechanisms by which insulin resistance influences HDL metabolism. Progress in our understanding of HDL metabolism and macrophage reverse cholesterol transport will increase the likelihood of developing novel therapies to raise plasma HDL concentrations and promote macrophage RCT and in proving that these new therapeutic interventions prevent or cause regression of atherosclerosis in humans.
Key Words: high density lipoprotein • insulin resistance • lipase • lipoprotein • reverse cholesterol transport
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