Review Articles
AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis
Authors:
Laurence Zhu ,
Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas, US
About Laurence
B.S.
Longhou Fang
Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas, US
About Longhou
Ph.D.
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.
How to Cite:
1. Zhu L, Fang L. AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis. Methodist DeBakey Cardiovascular Journal. 2015;11(3):160-165. DOI: http://doi.org/10.14797/mdcj-11-3-160
Published on
01 Jul 2015.
Peer Reviewed
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