Source:http://linkedlifedata.com/resource/pubmed/id/16408108
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-1-12
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pubmed:abstractText |
Renal fibrosis is the inevitable consequence of an excessive accumulation of extracellular matrix that occurs in virtually every type of chronic kidney disease. The pathogenesis of renal fibrosis is a progressive process that ultimately leads to end-stage renal failure, a devastating disorder that requires dialysis or kidney transplantation. In a simplistic view, renal fibrosis represents a failed wound-healing process of the kidney tissue after chronic, sustained injury. Several cellular pathways, including mesangial and fibroblast activation as well as tubular epithelial-mesenchymal transition, have been identified as the major avenues for the generation of the matrix-producing cells in diseased conditions. Among the many fibrogenic factors that regulate renal fibrotic process, transforming growth factor-beta (TGF-beta) is one that plays a central role. Although defective matrix degradation may contribute to tissue scarring, the exact action and mechanisms of the matrix-degrading enzymes in the injured kidney have become increasingly complicated. Recent discoveries on endogenous antifibrotic factors have evolved novel strategies aimed at antagonizing the fibrogenic action of TGF-beta/Smad signaling. Many therapeutic interventions appear effective in animal models; however, translation of these promising results into humans in the clinical setting remains a daunting task. This mini-review attempts to highlight the recent progress in our understanding of the cellular and molecular pathways leading to renal fibrosis, and discusses the challenges and opportunities in developing therapeutic strategies.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/BMP7 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein 7,
http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Hepatocyte Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Smad Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0085-2538
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
213-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16408108-Animals,
pubmed-meshheading:16408108-Bone Morphogenetic Protein 7,
pubmed-meshheading:16408108-Bone Morphogenetic Proteins,
pubmed-meshheading:16408108-Fibrosis,
pubmed-meshheading:16408108-Glomerulosclerosis, Focal Segmental,
pubmed-meshheading:16408108-Hepatocyte Growth Factor,
pubmed-meshheading:16408108-Humans,
pubmed-meshheading:16408108-Kidney,
pubmed-meshheading:16408108-Matrix Metalloproteinase 9,
pubmed-meshheading:16408108-Signal Transduction,
pubmed-meshheading:16408108-Smad Proteins,
pubmed-meshheading:16408108-Transforming Growth Factor beta
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pubmed:year |
2006
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pubmed:articleTitle |
Renal fibrosis: new insights into the pathogenesis and therapeutics.
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pubmed:affiliation |
Division of Cellular and Molecular Pathology, Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA. liuy@upmc.edu
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pubmed:publicationType |
Journal Article,
Review,
Research Support, N.I.H., Extramural
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