Skip Navigation

Nephrology Dialysis Transplantation 2007 22(9):2421-2425; doi:10.1093/ndt/gfm320
This Article
Right arrow Full Text Freely available
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 Related articles in NDT
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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Meier, M.
Right arrow Articles by Haller, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meier, M.
Right arrow Articles by Haller, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Nailing down PKC isoform specificity in diabetic nephropathy—two's company, three's a crowd

Matthias Meier, Jan Menne, Joon-Keun Park and Hermann Haller

Department of Nephrology, Hannover Medical School, Hannover, Germany

Correspondence and offprint requests to: Matthias Meier, MD, Department of Nephrology, Hannover Medical School, Carl-Neuberg-Strasse 1 30625 Hannover, Germany. Email: meier.matthias@mh-hannover.de

Keywords: dielectric nephropathy; protein kinase

The first 150 words of the full text of this article appear below.



   Introduction
 
Diabetic nephropathy is characterized by early vascular dysfunction and increasing matrix accumulation in the kidney, eventually leading to proteinuria, glomerulosclerosis and interstitial fibrosis [1]. Over the last decade, our understanding of the molecular mechanisms and the pathogenesis of diabetic nephropathy (and other diabetic microvascular complications) has been greatly enhanced [2]. However, we still do not completely understand how metabolic disturbances in the diabetic state, i.e. hyperglycaemia, induce such a vast array of distinct cellular events leading to progressive renal failure [2]. Several hypotheses linking hyperglycaemia and altered cellular biology have been proposed [3]. One of these hypotheses postulates that high glucose concentration leads to the activation of the calcium- and phospholipid-dependent protein kinase C (PKC) signalling pathway which subsequently mediates cellular response, e.g. with altered gene expression [4]. It is generally believed that intracellular PKC activation is achieved by the . . . [Full Text of this Article]



   PKC isoforms
 


   Conclusion
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related articles in NDT:

In this issue ...

NDT 2007 22: i. [Extract] [FREE Full Text]