Key result
ApoA-I binding protein (AIBP) augments HDL functionality by accelerating cholesterol efflux and inhibits vascular endothelial growth factor receptor 2 activation, limiting angiogenesis and potentially reducing atherosclerosis.
AIBP represents a potential novel therapeutic approach for coronary artery disease by accelerating reverse cholesterol transport and disrupting intraplaque angiogenesis.
May support novel RCT-targeted therapies in CAD; extends observational HDL data to causal interventional evidence.
Cardiovascular disease, which is often driven by hypercholesterolemia and subsequent coronary atherosclerosis, is the number-one 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.
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Zhu et al. (2015) conducted a review in Atherosclerosis and Coronary Artery Disease. ApoA-I binding protein (AIBP) was evaluated. ApoA-I binding protein (AIBP) augments HDL functionality by accelerating cholesterol efflux and inhibits vascular endothelial growth factor receptor 2 activation, limiting angiogenesis and potentially reducing atherosclerosis.
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