Linked Life Data

9919472

Source:http://linkedlifedata.com/resource/pubmed/id/9919472

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-3-22
pubmed:abstractText
Elevated plasma homocysteine is an independent risk factor for atherosclerosis and thrombosis. The exact mechanism by which homocysteine exerts its atherothrombotic action is still unclear. Accumulating evidence suggests that hyperhomocysteinaemia leads to endothelial injury and dysfunction, mediated by free radicals generated during the oxidation of homocysteine. Homocysteine also stimulates the proliferation of vascular smooth-muscle cells and inhibits the growth of vascular endothelial cells. Elevated homocysteine levels may also promote thrombosis by increased generation of thrombin. Other possible mechanisms for homocysteine-mediated atherogenesis include: the altered methylation of DNA and altered regulatory proteins associated with cell membrane, decreased bioavailability of nitric oxide, increased elastolysis and collagen accumulation, overstimulation of N-methyl-D-aspartate receptors and excessive adhesion of monocytes and neutrophils to endothelium. Understanding the mechanisms in vivo by which hyperhomocysteinaemia is associated with vascular disease may provide new approaches to prevention and treatment of atherothrombosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1350-6277
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
239-47
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Pathogenesis of vascular disease in hyperhomocysteinaemia.
pubmed:affiliation
Department of Medicine, University School of Medicine, Jagiellonian University, Cracow, Poland.
pubmed:publicationType
Journal Article, Review