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Updated: Jun 23, 2025

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
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TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review)

Jianchun Li1, Yuanxia Zou1, Jiraporn Kantapan1

  • 1Department of Radiologic Technology, Molecular Imaging and Therapy Research Unit, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai 50200, Thailand.

Molecular Medicine Reports
|June 21, 2024
PubMed

Insights

Post-translational modifications of the Transforming Growth Factor-beta (TGF-β)/Smad pathway are key in chronic kidney disease (CKD) fibrosis. Understanding these modifications offers new therapeutic targets for antifibrotic treatments in CKD.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cellular Biology

Background:

  • The Transforming Growth Factor-beta (TGF-β)/Smad signaling pathway is central to kidney fibrosis in chronic kidney disease (CKD).
  • Dysregulation of this pathway contributes to cellular processes implicated in CKD progression.

Purpose of the Study:

  • To review the post-translational modifications (PTMs) of the TGF-β/Smad pathway in the context of CKD.
  • To explore how PTMs influence TGF-β/Smad signaling and its role in renal pathophysiology.

Main Methods:

  • Literature review focusing on PTMs of TGF-β receptors and Smad proteins.
  • Analysis of studies investigating TGF-β/Smad pathway modulation in CKD models and patients.

Main Results:

  • PTMs, such as phosphorylation and ubiquitination, critically regulate TGF-β/Smad pathway activity, stability, and interactions.
  • These modifications impact renal tubular epithelial cell apoptosis, inflammation, myofibroblast activation, cellular aging, and autophagy in CKD.

Conclusions:

  • Detailed understanding of TGF-β/Smad pathway PTMs in CKD is crucial for developing targeted antifibrotic therapies.
  • Further research into these molecular mechanisms may yield novel treatments to preserve kidney function and integrity.
Keywords:
SmadsTGF‑βchronic kidney diseasefibrosispost‑translational modification

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