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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
14 Suppl
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pubmed:dateCreated |
2008-9-30
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pubmed:abstractText |
Vascular injury results in loss of endothelial nitric oxide (NO), production of reactive oxygen species (ROS), and the initiation of an inflammatory response. Both NO and ROS modulate inflammation through redox-sensitive pathways. Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) that regulates enzymatic synthesis of either nitric oxide or ROS. We hypothesized that endothelial BH4 is an important regulator of inflammation and vascular remodeling.
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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 |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/5,6,7,8-tetrahydrobiopterin,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins E,
http://linkedlifedata.com/resource/pubmed/chemical/Biopterin,
http://linkedlifedata.com/resource/pubmed/chemical/Ccr2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/GTP Cyclohydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR2,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1524-4539
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pubmed:author |
pubmed-author:AkhtarAsim MAM,
pubmed-author:AliZiad AZA,
pubmed-author:AlpNicholas JNJ,
pubmed-author:BendallJennifer KJK,
pubmed-author:BursillChristina ACA,
pubmed-author:ChannonKeith MKM,
pubmed-author:DouglasGillianG,
pubmed-author:GreavesDavid RDR,
pubmed-author:McNeillEileenE,
pubmed-author:PapaspyridonosMariannaM,
pubmed-author:TathamAmy LAL
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pubmed:issnType |
Electronic
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pubmed:day |
30
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pubmed:volume |
118
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S71-7
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pubmed:meshHeading |
pubmed-meshheading:18824773-Animals,
pubmed-meshheading:18824773-Aorta,
pubmed-meshheading:18824773-Apolipoproteins E,
pubmed-meshheading:18824773-Atherosclerosis,
pubmed-meshheading:18824773-Biopterin,
pubmed-meshheading:18824773-Blood Vessels,
pubmed-meshheading:18824773-Carotid Arteries,
pubmed-meshheading:18824773-Chemokine CCL2,
pubmed-meshheading:18824773-Chemotaxis,
pubmed-meshheading:18824773-Endothelium, Vascular,
pubmed-meshheading:18824773-Female,
pubmed-meshheading:18824773-GTP Cyclohydrolase,
pubmed-meshheading:18824773-Humans,
pubmed-meshheading:18824773-Hyperplasia,
pubmed-meshheading:18824773-Macrophages,
pubmed-meshheading:18824773-Male,
pubmed-meshheading:18824773-Mice,
pubmed-meshheading:18824773-Mice, Knockout,
pubmed-meshheading:18824773-Mice, Transgenic,
pubmed-meshheading:18824773-Nitric Oxide Synthase Type III,
pubmed-meshheading:18824773-Receptors, CCR2,
pubmed-meshheading:18824773-Superoxides,
pubmed-meshheading:18824773-Tunica Intima,
pubmed-meshheading:18824773-Up-Regulation,
pubmed-meshheading:18824773-Vasculitis,
pubmed-meshheading:18824773-Venae Cavae,
pubmed-meshheading:18824773-Wounds and Injuries
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pubmed:year |
2008
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pubmed:articleTitle |
CCR2-mediated antiinflammatory effects of endothelial tetrahydrobiopterin inhibit vascular injury-induced accelerated atherosclerosis.
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pubmed:affiliation |
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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