Document Detail


The role of tubular epithelial-mesenchymal transition in progressive kidney disease.
MedLine Citation:
PMID:  17587828     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The accumulation of interstitial matrix represents the final common pathway of most forms of kidney disease. Much of this matrix is synthesized by interstitial myofibroblasts, recruited from resident fibroblasts and circulating precursors. In addition, a significant proportion is derived from epithelial-mesenchymal transition (EMT) of tubuloepithelial cells. The importance of EMT has been demonstrated in experimental models, where blockade of EMT attenuates renal fibrosis. Although a number of factors may initiate EMT in the kidney, the most potent is transforming growth factor-beta1 (TGF-beta1). Moreover, many other prosclerotic factors have effects on EMT indirectly, via induction of TGF-beta1. Signaling events in this pathway include activation of Smad/integrin-linked kinase (ILK) and connective tissue growth factor (CTGF). Basement membrane integrity is also a key regulator of EMT. In particular, overexpression of matrix metalloproteinase-2 has a key role in the initiation of EMT, membrane dissolution, and the interstitial transit of transformed mesenchymal cells. Endogenous inhibitors of EMT also play an important counterregulatory role both to prevent EMT and stimulate uncommitted cells to regain their tubular phenotype (mesenchymal-epithelial transition). Such inhibitors represent a potential therapeutic approach, offering a mechanism to slow or even redress established renal fibrosis.
Authors:
W C Burns; P Kantharidis; M C Thomas
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Cells, tissues, organs     Volume:  185     ISSN:  1422-6421     ISO Abbreviation:  Cells Tissues Organs (Print)     Publication Date:  2007  
Date Detail:
Created Date:  2007-06-25     Completed Date:  2007-07-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100883360     Medline TA:  Cells Tissues Organs     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  222-31     Citation Subset:  IM    
Copyright Information:
2007 S. Karger AG, Basel
Affiliation:
Danielle Alberti Memorial Centre for Diabetes Complications, Baker Medical Research Institute, Melbourne, Australia. wendy.burns@baker.edu.au
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MeSH Terms
Descriptor/Qualifier:
Animals
Disease Progression
Epithelial Cells / metabolism,  pathology*
Humans
Kidney Diseases / metabolism,  pathology*
Kidney Tubules / metabolism,  pathology*
Mesoderm / metabolism,  pathology*

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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