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Updated: Jul 19, 2026
Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Perspectives on blockade of TGFbeta overexpression
Y Huang1, W A Border, N A Noble
1Fibrosis Research Laboratory, Division of Nephrology, University of Utah School of Medicine, Salt Lake City, 84108, USA.
Blocking TGF-beta signaling can slow kidney disease. New research shows that losing Smad corepressors Ski and SnoN amplifies TGF-beta
Area of Science:
- Nephrology
- Molecular Biology
- Fibrosis Research
Background:
- Transforming growth factor-beta (TGF-beta) signaling is a key driver of kidney fibrosis.
- Therapeutic strategies targeting TGF-beta-Smad pathways are being developed to treat progressive renal disease.
Discussion:
- Fukasawa et al. investigated the role of Smad corepressors Ski and SnoN in a unilateral ureteral obstruction model.
- Their findings identify the loss of Ski and SnoN as a critical mechanism that exacerbates TGF-beta-induced profibrotic responses in the kidney.
Key Insights:
- Loss of Smad corepressors Ski and SnoN potentiates TGF-beta's profibrotic effects.
- This provides a novel therapeutic target for managing kidney fibrosis.
Outlook:
- Further research into Smad corepressor function could reveal new therapeutic avenues for fibrotic kidney diseases.
- Understanding these mechanisms may lead to more effective treatments for patients with progressive renal conditions.
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