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Updated: Sep 3, 2025

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Transforming growth factor-β induced protein regulates pulmonary fibrosis via the G-protein signaling modulator 2

Kai Yang1, Na Huang1, Jian Sun2

  • 1Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Chengdu Medical College, No. 278, Baoguang Avenue, Xindu District, Chengdu, Sichuan 610500, China; Chengdu Medical College, No. 783, Xindu Avenue, Xindu District, Chengdu, Sichuan 610500, China.

Peptides
|July 25, 2022
PubMed

Insights

Transforming growth factor-beta induced protein (TGFBI) drives pulmonary fibrosis by altering G-protein signaling modulator 2 (GPSM2) and Snail. Targeting TGFBI offers a new therapeutic strategy for this severe lung disease.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Biochemistry

Background:

  • Pulmonary fibrosis is a progressive lung disease with limited treatment options.
  • It involves fibroblast activation and excessive extracellular matrix deposition, leading to respiratory failure.
  • Novel therapeutic targets are crucial for managing pulmonary fibrosis.

Purpose of the Study:

  • To investigate the role of transforming growth factor-beta induced protein (TGFBI) in pulmonary fibrosis.
  • To elucidate the mechanism by which TGFBI regulates fibrosis, focusing on the G-protein signaling modulator 2 (GPSM2)/Snail axis.

Main Methods:

  • Utilized bleomycin-induced rat models and TGF-beta1-stimulated human lung fibroblasts (IMR-90).
  • Employed siRNA to silence TGFBI and Snail, and overexpressed GPSM2.
  • Administered TGF-beta signaling inhibitor SB431542.

Main Results:

  • TGFBI expression was upregulated, while GPSM2 was downregulated in fibrotic lung tissues and cells.
  • Silencing TGFBI or inhibiting TGF-beta signaling reduced fibrotic effects and normalized GPSM2/Snail expression.
  • GPSM2 overexpression and Snail silencing also attenuated TGF-beta1-induced fibrosis.

Conclusions:

  • TGFBI promotes pulmonary fibrosis via the GPSM2/Snail pathway.
  • TGFBI represents a novel mediator and potential therapeutic target for pulmonary fibrosis.
Keywords:
G-protein signaling modulator 2Pulmonary fibrosisTransforming growth factor-βTransforming growth factor-β induced protein

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