Copyright
©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Nephrol. Jul 6, 2015; 4(3): 367-373
Published online Jul 6, 2015. doi: 10.5527/wjn.v4.i3.367
Published online Jul 6, 2015. doi: 10.5527/wjn.v4.i3.367
How tubular epithelial cells dictate the rate of renal fibrogenesis?
Kevin Louis, Alexandre Hertig, AP-HP, Hôpital Tenon, Urgences Néphrologiques et Transplantation Rénale, F-75020 Paris, France
Alexandre Hertig, UPMC Sorbonne Université Paris 06, UMR S 1155, F-75020 Paris, France
Author contributions: Both authors contributed to this manuscript.
Conflict-of-interest statement: I declare, as the corresponding author, that neither I nor Kevin Louis have any conflict of interest with regard to the manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Alexandre Hertig, Professor, UPMC Sorbonne Université Paris 06, UMR S 1155, 4 rue de la Chine, F-75020 Paris, France. alexandre.hertig@upmc.fr
Telephone: +33-15-6016695 Fax: +33-15-6017968
Received: February 10, 2015
Peer-review started: February 11, 2015
First decision: March 20, 2015
Revised: May 6, 2015
Accepted: May 16, 2015
Article in press: May 18, 2015
Published online: July 6, 2015
Peer-review started: February 11, 2015
First decision: March 20, 2015
Revised: May 6, 2015
Accepted: May 16, 2015
Article in press: May 18, 2015
Published online: July 6, 2015
Core Tip
Core tip: In this review, we explain why and how tubular epithelial cells should be regarded not only as victims in the context of chronic kidney disease, but also as actors playing an ambiguous role. In particular, we report on studies which demonstrated that they can actively contribute to fibrogenesis itself, either directly, because their function has been reprogrammed in a way reminiscent of their mesenchymal origin, or from a distance, by influencing endothelial and myofibroblast functions. Last, they are seen as potential targets for new drugs aiming at controlling fibrosis.