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NDT Advance Access originally published online on April 6, 2009
Nephrology Dialysis Transplantation 2009 24(7):2021-2023; doi:10.1093/ndt/gfp150
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Inhibition of protein kinase C in diabetic nephropathy—where do we stand?

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

Department of Nephrology, Hanover Medical School, Hanover, Germany

Correspondence and offprint requests to: Jan Menne; E-mail: menne.jan@mh-hannover.de

Keywords: diabetic nephropathy; protein kinase C

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

Hyperglycaemia plays a key role in the pathogenesis of microvascular diabetic complications. More than 20 years ago, it was described that the activation of the protein kinase C (PKC) system by hyperglycaemia may represent an important mediator of glucotoxicity in diabetic nephropathy [1,2]. The putative intracellular mechanism is the glucose-induced de novo synthesis of diacylglycerol that is one of the intracellular activators of PKC. Although hyperglycaemia is a major PKC activator, several other PKC stimuli related to the diabetic state such as increased production of reactive oxygen species, free fatty acids or various growth factors and angiotensin II have been identified over the last two decades [3,4] (Figure 1). Thus, inhibition of PKC to prevent complications of diabetes is an attractive hypothesis. However, there are several obstacles to such a strategy.


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  		Fig. 1 In the diabetic milieu, metabolic and haemodynamic factors lead to PKC activation and vice . . . [Full Text of this Article]

 

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