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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PMC:4666422Le document en format XML
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<author><name sortKey="Zhu, Laurence" sort="Zhu, Laurence" uniqKey="Zhu L" first="Laurence" last="Zhu">Laurence Zhu</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis</title>
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<series><title level="j">Methodist DeBakey Cardiovascular Journal</title>
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<front><div type="abstract" xml:lang="en"><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>
</div>
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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>
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<issn pub-type="ppub">1947-6094</issn>
<issn pub-type="epub">1947-6108</issn>
<publisher><publisher-name>The Methodist Hospital Houston, Texas</publisher-name>
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<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>
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<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>
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<aff id="aff1">Houston Methodist Research Institute, Houston Methodist Hospital, Houston, Texas</aff>
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<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>
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<counts><page-count count="6"></page-count>
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