TGF-beta signal transduction in chronic kidney disease.

Abstract

Transforming growth factor (TGF)-beta is a central stimulus of the events leading to chronic progressive kidney disease, having been implicated in the regulation of cell proliferation, hypertrophy, apoptosis and fibrogenesis. The fact that it mediates these varied events suggests that multiple mechanisms play a role in determining the outcome of TGF-beta signaling. Regulation begins with the availability and activation of TGF-beta and continues through receptor expression and localization, control of the TGF-beta family-specific Smad signaling proteins, and interaction of the Smads with multiple signaling pathways extending into the nucleus. Studies of these mechanisms in kidney cells and in whole-animal experimental models, reviewed here, are beginning to provide insight into the role of TGF-beta in the pathogenesis of renal dysfunction and its potential treatment.

050100150200920102011201220132014201520162017
Citations per Year

526 Citations

Semantic Scholar estimates that this publication has 526 citations based on the available data.

See our FAQ for additional information.

Cite this paper

@article{Schnaper2009TGFbetaST, title={TGF-beta signal transduction in chronic kidney disease.}, author={H . William Schnaper and Sara Jandeska and Constance E. Runyan and Susan C. Hubchak and Rajit K. Basu and Jessica F Curley and Ronald D Smith and Tomoko Hayashida}, journal={Frontiers in bioscience}, year={2009}, volume={14}, pages={2448-65} }