rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2011-3-18
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pubmed:abstractText |
Phosphatidylcholine (PC) is the predominant phospholipid component of circulating lipoproteins. The majority of PC is formed by the choline pathway. However, approximately one-third of hepatic PC can also be synthesized by phosphatidylethanolamine N-methyltransferase (PEMT). PEMT is required for normal secretion of very-low-density lipoproteins from the liver. We hypothesized that lack of PEMT would attenuate atherosclerosis and improve myocardial function.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
1524-4571
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pubmed:author |
|
pubmed:issnType |
Electronic
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pubmed:day |
18
|
pubmed:volume |
108
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
686-94
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pubmed:meshHeading |
pubmed-meshheading:21273556-Aging,
pubmed-meshheading:21273556-Animals,
pubmed-meshheading:21273556-Aorta,
pubmed-meshheading:21273556-Apolipoproteins E,
pubmed-meshheading:21273556-Atherosclerosis,
pubmed-meshheading:21273556-Cholesterol,
pubmed-meshheading:21273556-Heart,
pubmed-meshheading:21273556-Heart Diseases,
pubmed-meshheading:21273556-Lipid Metabolism,
pubmed-meshheading:21273556-Lipoproteins,
pubmed-meshheading:21273556-Liver,
pubmed-meshheading:21273556-Mice,
pubmed-meshheading:21273556-Mice, Knockout,
pubmed-meshheading:21273556-Myocardium,
pubmed-meshheading:21273556-Phosphatidylcholines,
pubmed-meshheading:21273556-Phosphatidylethanolamine N-Methyltransferase,
pubmed-meshheading:21273556-Triglycerides
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pubmed:year |
2011
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pubmed:articleTitle |
Impaired phosphatidylcholine biosynthesis reduces atherosclerosis and prevents lipotoxic cardiac dysfunction in ApoE-/- Mice.
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pubmed:affiliation |
Molecular and Cell Biology of Lipids and Department of Biochemistry, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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