Source:http://linkedlifedata.com/resource/pubmed/id/16709942
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2006-7-21
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pubmed:abstractText |
BACKGROUND: Over the past 10 to 15 years, calcific aortic valve disease, which includes aortic sclerosis and aortic stenosis, has come to be recognized as an active process, based on: (1) epidemiologic studies demonstrating associations of specific risk factors with increased prevalence or rate of progression of aortic valve disease; (2) identification, in valve lesions, of histopathologic features of chronic inflammation, lipoprotein deposition, renin-angiotensin system components, and molecular mediators of calcification; and (3) identification of cell-signaling pathways and genetic factors that may participate in valve disease pathogenesis. These studies will be reviewed and organized into a proposed global hypothesis for the pathogenesis of calcific aortic valve disease.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1524-4636
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
26
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1721-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading | |
pubmed:year |
2006
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pubmed:articleTitle |
Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more).
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pubmed:affiliation |
Division of Cardiology, Box 356422, University of Washington, Seattle, WA 98195-6422, USA. cardiac@u.washington.edu
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pubmed:publicationType |
Journal Article,
Review,
Research Support, N.I.H., Extramural
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