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Updated: Jan 27, 2026
Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
The many talents of transforming growth factor-β in the kidney
Leslie Gewin1,2,3
1Division of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center.
Purpose Of Review:
Preclinical data suggests that transforming growth factor-β (TGF-β) is arguably the most potent profibrotic growth factor in kidney injury. Despite this, recent clinical trials targeting TGF-β have been disappointing. These negative studies suggest that TGF-β signaling in the injured kidney might be more complicated than originally thought. This review examines recent studies that expand our understanding of how this pleiotropic growth factor affects renal injury.
Recent Findings:
There are recent studies showing new mechanisms whereby TGF-β can mediate injury (e.g. epigenetic effects, macrophage chemoattractant). However, more significant are the increasing reports on cross-talk between TGF-β signaling and other pathways relevant to renal injury such as Wnt/β-catenin, YAP/TAZ (transcriptional coactivator with PDZ-binding motif), and klotho/FGF23. TGF-β clearly alters the response to injury, not just by direct transcriptional changes on target cells, but also through effects on other signaling pathways. In T cells and tubular epithelial cells, some of these TGF-β-mediated changes are potentially beneficial.
Summary:
It is unlikely that inhibition of TGF-β per se will be a successful antifibrotic strategy, but a better understanding of TGF-β's actions may reveal promising downstream targets or modulators of signaling to target therapeutically for chronic kidney disease.
Insights
Transforming growth factor-β (TGF-β) plays a complex role in kidney injury. Targeting TGF-β alone may not be effective, but understanding its interactions reveals new therapeutic strategies for chronic kidney disease.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Signaling
Background:
- Transforming growth factor-β (TGF-β) is a potent profibrotic factor in preclinical kidney injury models.
- Recent clinical trials targeting TGF-β in kidney disease have yielded disappointing results.
- This suggests a more complex role for TGF-β signaling in renal injury than previously understood.
Purpose of the Study:
- To review recent studies that enhance the understanding of TGF-β's role in renal injury.
- To explore novel mechanisms of TGF-β-mediated kidney damage.
- To examine the cross-talk between TGF-β and other critical signaling pathways in kidney disease.
Main Methods:
- Literature review of recent preclinical and clinical studies.
- Analysis of emerging mechanisms of TGF-β action.
- Examination of signaling pathway interactions in renal injury.
Main Results:
- New TGF-β-mediated injury mechanisms include epigenetic effects and macrophage chemoattraction.
- Significant cross-talk exists between TGF-β and pathways like Wnt/β-catenin, YAP/TAZ, and klotho/FGF23.
- TGF-β influences renal injury response through direct transcriptional changes and modulation of other signaling pathways, with some effects potentially beneficial.
Conclusions:
- Direct inhibition of TGF-β is unlikely to be a successful antifibrotic strategy for chronic kidney disease.
- A deeper understanding of TGF-β's complex actions and interactions is crucial.
- Identifying downstream targets or signaling modulators offers promising therapeutic avenues for chronic kidney disease.
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