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
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
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| Introduction |
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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].
| PAX Family |
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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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