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NDT Advance Access published online on September 26, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn533
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Does TNF-{alpha} enhance cystogenesis in ADPKD?*

Yves Pirson

Division of Nephrology, Cliniques Universitaires Saint-Luc and Université catholique de Louvain Medical School, B-1200 Brussels, Belgium

Correspondence and offprint requests to: Prof. Y. Pirson, Service de Néphrologie, Cliniques Universitaires Saint-Luc, Av. Hippocrate, 10, B-1200 BRUXELLES. Tel: +32-2-7641857; Fax: +32-2-7642836; E-mail: yves.pirson@uclouvain.be

Keywords: autosomal dominant polycystic kidney disease; autosomal recessive polycystic kidney disease; ethanercept; FIP-2; TNF-{alpha}

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



   Unravelling nongenetic factors contributing to cystogenesis in ADPKD
 
Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutation in either PKD1 (85%) or PKD2 (15%) genes. The resulting disease phenotypes are very similar, except that renal disease is typically less severe in PKD2 families [1].

The protein products of PDK1 and PKD2, polycystin-1 (PC-1) and polycystin-2 (PC-2), are membrane proteins that probably form a functional complex [1]. PC-1 is regarded as a receptor for an unidentified ligand while PC-2 has significant homology to the transient receptor potential (TRP) family of store-operated calcium channels and is likely to function similarly as a non-selective calcium channel [1–3]. Like many other proteins implicated in renal cystic diseases, PC-1 and PC-2 are located in the primary cilium, a single hair-like organelle projecting from the surface of most mammalian cells. In tubular epithelial cells, the cilium projects into the lumen and is thought to act as . . . [Full Text of this Article]



   Exploring TNF-{alpha}-mediated pathway as an enhancer of ADPKD
 


   Revealing a pathway connecting TNF-{alpha} signalling, polycystins and cystogenesis
 
Weighing potential clinical implications of this work
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