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NDT Advance Access published online on June 25, 2009

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp307
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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



Renal recovery after injury: the role of Pax-2

Rafael S. Lindoso*, Karine S. Verdoorn* and Marcelo Einicker-Lamas

Laboratório de Fisico-Química Biológica Aída Hasson Voloch, Instituto de Biofísica Carlo Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

Correspondence and offprint requests to: Marcelo Einicker-Lamas; E-mail: einicker@biof.ufrj.br

Keywords: kidney disease; Pax-2; renal regeneration; signalling

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



   Introduction
 
Tubular epithelial cells often suffer injury and damage caused by different factors such as ischaemia or toxicity (for review, see [1,2]). From the observations in human studies and animal models, it is clear that these acute insults can result in chronic kidney disease [3]. The structural and functional restoration of the kidney depends on a delicate balance of growth and transcription factors that guide gene expression [4]. The signalling pathways triggered during this process often resemble those observed during kidney development.

Tissue regeneration comprises dedifferentiation, proliferation and transdifferentiation processes [5]. After injury, surviving cells suffer dedifferentiation assuming progenitor cell characteristics (epithelial-to-mesenchymal transition) [6]. Indeed, markers of undifferentiated cells are re-expressed such as vimentin, which occurs in mesenchymal cells and not in mature cells [7], and neural cell adhesion molecules expressed initially in the metanephric mesenchyme [8]. . . . [Full Text of this Article]



   PAX Family
 
PAX-2 in kidney development and repair
PAX-2 upregulation: the renin–angiotensin system (RAS)
PAX-2 downregulation: activin A


   Future Perspectives
 

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