| Literature DB >> 19273211 |
H William Schnaper1, Sara Jandeska, Constance E Runyan, Susan C Hubchak, Rajit K Basu, Jessica F Curley, Ronald D Smith, Tomoko Hayashida.
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.Entities:
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Year: 2009 PMID： 19273211 PMCID： PMC4367189 DOI： 10.2741/3389
Source DB: PubMed Journal: Front Biosci (Landmark Ed) ISSN： 2768-6698