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Daniel J. Rader, MD

JAMA. 2003;290:2322-2324.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Plasma levels of high-density lipoprotein cholesterol (HDL-C) and its major protein apolipoprotein A-I (apoA-I) are consistently inversely associated with coronary heart disease (CHD) risk in observational studies.¹ Furthermore, studies in animals over the last 2 decades have established that intravenous infusion of HDL or apoA-I or genetic overexpression of apoA-I can substantially reduce the progression and even induce regression of preexisting atherosclerosis.² Based on these data, HDL and apoA-I have become a major target for the development of new therapies for atherosclerosis.^3-4

Finding small molecules that upregulate the gene expression of apoA-I has been an elusive goal of pharmaceutical research for more than 2 decades. Despite intensive investigation, few compounds that upregulate apoA-I have been found and none have entered large-scale clinical trials, leading to increasing interest in other modalities to deliver apoA-I therapeutically. Given that administration of recombinant proteins is an established therapeutic approach for . . . [Full Text of this Article]

Author Affiliations: Department of Medicine and Center for Experimental Therapeutics, University of Pennsylvania School of Medicine, Philadelphia.

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