| Evidence for a role of phospholipid oxidation products in atherogenesis. | |
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MedLine Citation:
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PMID: 11686004 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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There is growing evidence for the accumulation of phospholipid oxidation products (some of which can also be formed enzymatically) in several chronic disease processes including atherosclerosis. There also is considerable evidence that enzymes involved in hydrolysis of these phospholipids (present in both lipoproteins and cells) may be important in regulation of atherogenesis. In vitro studies suggest that these lipids can activate vascular wall cells to states that contribute to the atherosclerotic process. This review focuses on two types of bioactive phospholipids: phosphatidyl cholines in which the sn-2 fatty acid has been modified by oxidation and lysophosphatidic acid in which both the sn-2 and sn-3 positions have been modified. The mechanism by which these phospholipid oxidation products activate cells has revealed the presence of several different receptors and signal transduction pathways. |
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Authors:
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J A Berliner; G Subbanagounder; N Leitinger; A D Watson; D Vora |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Trends in cardiovascular medicine Volume: 11 ISSN: 1050-1738 ISO Abbreviation: Trends Cardiovasc. Med. Publication Date: 2001 Apr-May |
Date Detail:
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Created Date: 2001-10-31 Completed Date: 2002-01-16 Revised Date: 2005-11-16 |
Medline Journal Info:
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Nlm Unique ID: 9108337 Medline TA: Trends Cardiovasc Med Country: United States |
Other Details:
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Languages: eng Pagination: 142-7 Citation Subset: IM |
Affiliation:
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Departments of Medicine and Pathology, UCLA School of Medicine, Los Angeles, California, USA. jberliner@mednet.ucla.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arteriosclerosis / etiology*, metabolism* Humans Molecular Structure Oxidation-Reduction Phospholipids / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Phospholipids |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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