Linked Life Data

15063353

Source:http://linkedlifedata.com/resource/pubmed/id/15063353

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-4-5
pubmed:abstractText
Overproduction of reactive oxygen species or increased oxidative stress is considered a major mechanism involved in the pathogenesis of endothelial dysfunction, the initiation and progression of atherosclerosis and its adverse events. Evidence supports the importance of nitric oxide derived from endothelial nitric oxide synthase as a vasoprotective substance, and of vascular NAD(P)H oxidase-derived reactive oxygen species as important signaling molecules in vascular cells. Recent studies show that dysfunction of endothelial nitric oxide synthase in atherosclerosis generates O(2)(-) rather than nitric oxide, and that upregulation of vascular NAD(P)H oxidase is closely associated with atherosclerotic progression and plaque instability.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1471-4892
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
110-5
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Oxidant stress and atherosclerosis.
pubmed:affiliation
Cardiovascular Division, Department of Medicine, Kobe University Graduate School of Medicine, 5-1.7-Chome, Kusunoki-Cho, Chuo-ku, Kobe, 650-0017, Japan. yokohama@med.kobe-u.ac.jp
pubmed:publicationType
Journal Article, Review