Authors:

Abstract

Cardiovascular disease, which is often driven by hypercholesterolemia and subsequent coronary atherosclerosis, is the numberone cause of morbidity and mortality in the United States. Based on long-term epidemiological studies, high-density lipoprotein cholesterol (HDL-C) levels are inversely correlated with risk for coronary artery disease (CAD). HDL-mediated reverse cholesterol transport (RCT) is responsible for cholesterol removal from the peripheral tissues and return to the liver for final elimination.¹ In atherosclerosis, intraplaque angiogenesis promotes plaque growth and increases plaque vulnerability. Conceivably, the acceleration of RCT and disruption of intraplaque angiogenesis would inhibit atherosclerosis and reduce CAD. We have identified a protein called apoA-I binding protein (AIBP) that augments HDL functionality by accelerating cholesterol efflux. Furthermore, AIBP inhibits vascular endothelial growth factor receptor 2 activation in endothelial cells and limits angiogenesis.² The following discusses the prospect of using AIBP as a novel therapeutic approach for the treatment of CAD.

Keywords: apoA-I binding protein, AIBP, angiogenesis, lymphangiogenesis, cholesterol efflux, reverse cholesterol transport