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Updated: Feb 10, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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Published on: August 3, 2018

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Transforming growth factor-β signalling in renal fibrosis: from Smads to non-coding RNAs

Patrick Ming-Kuen Tang1,2, Ying-Ying Zhang2,3, Thomas Shiu-Kwong Mak2

  • 1Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR, China.

The Journal of Physiology
|May 22, 2018
PubMed

Insights

Transforming growth factor-β (TGF-β) drives kidney fibrosis by altering non-coding RNAs. Targeting Smad3-dependent long non-coding RNAs offers potential precision therapies for chronic kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • Transforming growth factor-β (TGF-β) is a key mediator of tissue fibrosis.
  • Antifibrotic therapies targeting TGF-β may cause side effects due to its diverse physiological roles.
  • Understanding TGF-β signaling in fibrogenesis is crucial for identifying precise therapeutic targets.

Purpose of the Study:

  • To review the mechanisms of TGF-β-driven renal fibrosis.
  • To explore the role of non-coding RNAs in TGF-β-mediated fibrogenesis.
  • To discuss the translational potential of novel therapeutic targets in chronic kidney disease.

Main Methods:

  • Review of existing literature on TGF-β signaling pathways.
  • Analysis of Smad signaling pathways (Smad2, Smad3, Smad7) in renal fibrosis.
  • Investigation of non-coding RNA regulation in TGF-β-induced fibrosis.

Main Results:

  • Smad3 is pathogenic, while Smad2 and Smad7 are protective in TGF-β-mediated renal fibrosis.
  • TGF-β/Smad3 signaling alters microRNA profiles, promoting fibrosis by regulating non-coding RNAs.
  • Disease-specific Smad3-dependent long non-coding RNAs have been identified in kidney disease models.

Conclusions:

  • Non-coding RNAs are critical mediators of TGF-β-driven renal fibrosis.
  • Smad3-dependent long non-coding RNAs represent promising precision therapeutic targets for chronic kidney disease.
  • Further research into these non-coding RNAs could lead to novel antifibrotic strategies.
Keywords:
TGF-β/Smad3 signalingnon-coding RNAtissue fibrosis

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