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
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