AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis
Identifieur interne : 000302 ( Pmc/Curation ); précédent : 000301; suivant : 000303AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis
Auteurs : Laurence Zhu [États-Unis] ; Longhou Fang [États-Unis]Source :
- Methodist DeBakey Cardiovascular Journal [ 1947-6094 ] ; 2015.
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.
Url:
DOI: 10.14797/mdcj-11-3-160
PubMed: 26634023
PubMed Central: 4666422
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Methodist Debakey Cardiovasc J</journal-id><journal-id journal-id-type="iso-abbrev">Methodist Debakey Cardiovasc J</journal-id><journal-id journal-id-type="publisher-id">mdcj</journal-id><journal-title-group><journal-title>Methodist DeBakey Cardiovascular Journal</journal-title></journal-title-group><issn pub-type="ppub">1947-6094</issn><issn pub-type="epub">1947-6108</issn><publisher><publisher-name>The Methodist Hospital Houston, Texas</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26634023</article-id><article-id pub-id-type="pmc">4666422</article-id><article-id pub-id-type="doi">10.14797/mdcj-11-3-160</article-id><article-id pub-id-type="sici">i1947-6094-11-3-160</article-id><article-categories><subj-group subj-group-type="heading"><subject>New Concepts and Therapies for Atherosclerosis</subject></subj-group></article-categories><title-group><article-title>AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Zhu</surname><given-names>Laurence</given-names></name><degrees>B.S.</degrees><xref ref-type="aff" rid="aff1"></xref></contrib><contrib contrib-type="author"><name><surname>Fang</surname><given-names>Longhou</given-names></name><degrees>Ph.D.</degrees><xref ref-type="aff" rid="aff1"></xref></contrib><aff id="aff1">Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas</aff></contrib-group><pub-date pub-type="ppub"><season>Jul-Sep</season><year>2015</year></pub-date><volume>11</volume><issue>3</issue><fpage>160</fpage><lpage>165</lpage><permissions><copyright-statement>© 2015 The Methodist Hospital Houston, Texas</copyright-statement><copyright-year>2015</copyright-year></permissions><abstract><p>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.<xref rid="i1947-6094-11-3-160-b1" ref-type="bibr">1</xref> 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.<xref rid="i1947-6094-11-3-160-b2" ref-type="bibr">2</xref> The following discusses the prospect of using AIBP as a novel therapeutic approach for the treatment of CAD.</p></abstract><kwd-group><kwd>apoA-I binding protein</kwd><kwd>AIBP</kwd><kwd>angiogenesis</kwd><kwd>lymphangiogenesis</kwd><kwd>cholesterol efflux</kwd><kwd>reverse cholesterol transport</kwd></kwd-group><counts><page-count count="6"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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