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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2004-11-19
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pubmed:abstractText |
Hyperglycaemia is a primary cause of vascular complications in diabetes. A hallmark of these vascular complications is endothelial cell dysfunction, which is partly due to the reduced production of nitric oxide. The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/NOS3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrites,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0012-186X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1727-34
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15490108-Animals,
pubmed-meshheading:15490108-Aorta, Thoracic,
pubmed-meshheading:15490108-Cells, Cultured,
pubmed-meshheading:15490108-DNA Primers,
pubmed-meshheading:15490108-Endothelium, Vascular,
pubmed-meshheading:15490108-Glucose,
pubmed-meshheading:15490108-Humans,
pubmed-meshheading:15490108-Hyperglycemia,
pubmed-meshheading:15490108-Male,
pubmed-meshheading:15490108-Mice,
pubmed-meshheading:15490108-Mice, Inbred C57BL,
pubmed-meshheading:15490108-Mice, Mutant Strains,
pubmed-meshheading:15490108-Mutagenesis, Site-Directed,
pubmed-meshheading:15490108-Nitric Oxide Synthase,
pubmed-meshheading:15490108-Nitric Oxide Synthase Type II,
pubmed-meshheading:15490108-Nitric Oxide Synthase Type III,
pubmed-meshheading:15490108-Nitrites,
pubmed-meshheading:15490108-Polymerase Chain Reaction,
pubmed-meshheading:15490108-RNA, Messenger,
pubmed-meshheading:15490108-Reactive Oxygen Species,
pubmed-meshheading:15490108-Superoxides,
pubmed-meshheading:15490108-Transcription Factor AP-1
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pubmed:year |
2004
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pubmed:articleTitle |
Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells.
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pubmed:affiliation |
Division of Endocrinology and Metabolism, Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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