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Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15

  • 0The Affiliated Dongguan Songshan Lake Central Hospital, Guangdong Medical University, Dongguan, China.
Journal of Cellular and Molecular Medicine +

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August 22, 2025

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August 22, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Cinobufotalin (CB) shows promise in treating pulmonary fibrosis (PF) by inhibiting peptidase inhibitor 15 (PI15) and regulating key signaling pathways. This study identifies CB as a potential therapeutic candidate for PF patients.

Area Of Science

  • Pulmonary Medicine
  • Pharmacology
  • Molecular Biology

Background

  • Pulmonary fibrosis (PF) is a severe interstitial lung disease (ILD) with limited treatment options.
  • Cinobufotalin (CB), a small molecule, has shown anti-cancer properties.
  • Transforming growth factor-beta 1 (TGF-β1) signaling drives fibrosis through myofibroblast activation and epithelial-mesenchymal transition (EMT).

Purpose Of The Study

  • To investigate the therapeutic potential of cinobufotalin (CB) in pulmonary fibrosis (PF).
  • To elucidate the molecular mechanisms underlying CB's anti-fibrotic effects.
  • To identify novel molecular targets for PF treatment.

Main Methods

  • Bleomycin (BLM)-induced mouse model of PF.
  • In vitro studies on TGF-β1-induced myofibroblast activation and EMT.
  • Comparative RNA sequencing (RNA-Seq) for gene expression analysis.
  • Mechanistic studies on the TGF-β/Smad signaling pathway.

Main Results

  • CB treatment attenuated BLM-induced PF.
  • CB inhibited TGF-β1-induced myofibroblast activation and EMT.
  • Peptidase inhibitor 15 (PI15) was identified as a significantly differentially expressed gene in PF.
  • CB exerted anti-fibrotic effects by inhibiting PI15 and regulating the TGF-β/Smad pathway.

Conclusions

  • Cinobufotalin (CB) demonstrates significant anti-fibrotic effects in a preclinical model.
  • CB acts by inhibiting PI15 and modulating the TGF-β/Smad signaling pathway.
  • CB is a promising therapeutic candidate for pulmonary fibrosis.

Keywords:

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