Linked Life Data

15596110

Source:http://linkedlifedata.com/resource/pubmed/id/15596110

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-12-14
pubmed:abstractText
In vascular disease states such as atherosclerosis and diabetes, endothelial nitric oxide (NO) bioactivity is reduced and oxidative stress is increased, resulting in endothelial dysfunction. Recent studies suggest that changes in the activity and regulation of endothelial NO synthase by its cofactor tetrahydrobiopterin (BH4) is an important contributor to endothelial dysfunction. Pharmacologic studies and more recent insights from genetically modified mouse models have improved the understanding of the mechanistic role and importance of BH4 in vascular disease pathogenesis. Targeting BH4 may provide new therapeutic strategies in vascular disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1050-1738
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
323-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Tetrahydrobiopterin: regulator of endothelial nitric oxide synthase in vascular disease.
pubmed:affiliation
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom. keith.channon@cardiov.ox.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't