Published online Jul 6, 2015. doi: 10.5527/wjn.v4.i3.367
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: 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.