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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1996-10-25
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pubmed:abstractText |
The development of progressive tubular atrophy and interstitial fibrosis represents a final common pathway leading to renal insufficiency. My laboratory has been investigating several rat models of primary glomerular disease in an effort to determine cellular and molecular mechanisms of renal interstitial fibrosis. These models include puromycin aminonucleoside nephrosis (PAN), protein-overload proteinuria, passive Heymann nephritis, and diet-induced hypercholesterolemia. From a functional perspective, it is likely that the associated loss of tubules accounts for the decline in renal function. Four recurrent themes are emerging from our studies.
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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 |
May
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pubmed:issn |
0098-6577
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S49-54
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8731195-Animals,
pubmed-meshheading:8731195-Fibrosis,
pubmed-meshheading:8731195-Gene Expression Regulation,
pubmed-meshheading:8731195-Humans,
pubmed-meshheading:8731195-Nephritis, Interstitial,
pubmed-meshheading:8731195-Proteinuria,
pubmed-meshheading:8731195-Rats,
pubmed-meshheading:8731195-Up-Regulation
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pubmed:year |
1996
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pubmed:articleTitle |
Expression of genes that promote renal interstitial fibrosis in rats with proteinuria.
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pubmed:affiliation |
Division of Nephrology, Hospital for Sick Children, University of Toronto, Ontario, Canada.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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