Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 14, Issue -, Pages 2448-2465Publisher
BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/3389
Keywords
TGF-beta; Fibrosis; Signal Transduction; Smad; Cross-Talk; Review
Categories
Funding
- NIDDK [R01 DK49362, R01 DK75663]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK049362, R01DK075663] Funding Source: NIH RePORTER
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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 wholeanimal 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.
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