High-density lipoproteins (HDLs) are strongly related to risk of atherosclerotic cardiovascular disease. Low levels of HDL cholesterol are a major cardiovascular risk fac-tor, and overexpression of the major HDL protein, apo-lipoprotein (apo) A-I, markedly inhibits progression and even induces regression of atherosclerosis in animal models. Clinical data regarding the effect of increasing HDL cholesterol on vascular events are limited. HDL re-mains an important potential target for therapeutic in-tervention. A variety of gene products are involved in the regulation of HDL metabolism. Yet, the mechanisms by which HDL inhibits atherosclerosis are not yet fully un-derstood. There remains much to be learned about HDL metabolism and its relation to atherosclerosis and other cardiovascular risk factors. ᮊ2002 by Excerpta Med-ica, Inc. Am J Cardiol 2002;90(suppl):62i–70i T
CITATION STYLE
Rader, D. J. (2002). Atherosclerosis METABOLISM. October, 9149(02).
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