Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Mogyorosi, A.
Right arrow Articles by Ziyadeh, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mogyorosi, A.
Right arrow Articles by Ziyadeh, F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrology Dialysis Transplantation, Vol 14, Issue 5 1078-1081, Copyright © 1999 by Oxford University Press

INVITED COMMENTS

What is the role of decorin in diabetic kidney disease?

A Mogyorosi and F Ziyadeh
Division of Nephrology, Department of Medicine, Virginia Commonwealth University/Medical College of Virginia and McGuire VAMC, Richmond, Virginia, USA; Renal-Electrolyte and Hypertension Division, Department of Medicine, and the Penn Center for the Molecular Studies of Kidney Diseases, University of Pennsylvania, 415 Curie Boulevard, 700 Clinical Research Building, Philadelphia, PA 19104-6144, USA; Corresponding author

The small proteoglycan decorin may intercept the activity of the TGF-{beta} system. Decorin administration has been advocated as potential therapy in renal fibrotic diseases, because of the findings of a relative deficiency of decorin and a relative excess of TGF-{beta} in acute glomerulonephritis. Does a similar situation pertain in diabetic kidney disease? Activation of TGF-{beta} seems to be crucial to tissue injury in diabetic nephropathy, but until recently it has not been established whether decorin plays any role in the manifestations of this disease. We review evidence that a surfeit rather than a deficit in decorin expression exists in diabetic renal disease, and that there exists a negative feed-back loop whereby TGF-{beta}1 induces down-regulation of decorin expression. Rat and mouse mesangial cells as well as mouse proximal tubular cells in culture exhibit increased decorin mRNA levels in high ambient glucose. Decorin mRNA level in the kidney of streptozotocin-induced diabetes in mice is rapidly and significantly increased following the induction of diabetes. Thus, the available evidence suggests that renal decorin is not deficient in this disorder and hence decorin supplementation does not seem to be warranted. Rather, interception of the effects of TGF-{beta} seems to be an approach most likely to yield beneficial results in diabetic nephropathy. Keywords: diabetic nephropathy; extracellular matrix; fibrosis; glomerulopathy; proteoglycan; transforming growth factor-{beta}
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Exp. Biol. Med.Home page
J. Cheng and J. P. Grande
Transforming Growth Factor-{beta} Signal Transduction and Progressive Renal Disease
Experimental Biology and Medicine, December 1, 2002; 227(11): 943 - 956.
[Abstract] [Full Text]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.