Linked Life Data

13679676

Source:http://linkedlifedata.com/resource/pubmed/id/13679676

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2003-9-24
pubmed:abstractText
Endothelial dysfunction (ECD) is the earliest phenotypic change in the vasculature following exposure to atherothrombotic risk factors. ECD is associated with decreased synthesis and increased oxidative inactivation of nitric oxide (NO). Critical antioxidant enzymes essential for eliminating reactive oxygen species that can inactivate NO include the superoxide dismutases, the glutathione peroxidases, catalase, and glucose-6-phosphate dehydrogenase. Deficiencies of these enzymes increase oxidative stress and NO inactivation and, as such, can either lead to ECD or account for the underlying mechanism of ECD associated with a given atherothrombotic risk factor. Selected antioxidants improve intracellular redox state and reverse ECD by improving the bioavailability of NO. These observations provide mechanistic insights into the molecular basis of ECD in vascular disease and its treatment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1424-8832
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
359-60
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
Oxidative stress in endothelial cell dysfunction and thrombosis.
pubmed:affiliation
Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA. jloscalz@bu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review