AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis

Laurence Zhu, Longhou Fang

Research output: Contribution to journalReview article

9 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)160-165
Number of pages6
JournalMethodist DeBakey cardiovascular journal
Volume11
Issue number3
DOIs
StatePublished - Sep 30 2015

Keywords

  • AIBP
  • angiogenesis
  • apoA-I binding protein
  • cholesterol efflux
  • lymphangiogenesis
  • reverse cholesterol transport

ASJC Scopus subject areas

  • Medicine(all)

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