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Connective-Tissue Growth Factor Contributes to TGF-β1-induced Lung Fibrosis.

Toyoshi Yanagihara1,2,3, Kazuya Tsubouchi1,2, Mahsa Gholiof1

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American Journal of Respiratory Cell and Molecular Biology
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Connective-tissue growth factor (CTGF) drives pulmonary fibrosis by increasing myofibroblast accumulation. Inhibiting CTGF with pamrevlumab shows potential for treating this fatal lung disease.

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Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Molecular Biology

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease marked by excessive myofibroblast accumulation.
  • Connective-tissue growth factor (CTGF) is known to worsen lung fibrosis.
  • CTGF's role in IPF pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role of CTGF in a rat model of pulmonary fibrosis induced by AdTGF-β1.
  • To examine CTGF expression in IPF patients.
  • To evaluate the therapeutic potential of CTGF inhibition in pulmonary fibrosis.

Main Methods:

  • Induction of pulmonary fibrosis in rats using an adenovirus vector encoding active TGF-β1 (AdTGF-β1).
  • Quantification of CTGF expression in lung tissue, vascular smooth muscle cells, and endothelial cells.
  • Assessment of CTGF and TGF-β synergistic effects on fibroblast profibrotic markers.
  • Evaluation of pamrevlumab, a CTGF inhibitory antibody, in the fibrosis model.

Main Results:

  • CTGF was significantly upregulated in the AdTGF-β1-induced rat lung fibrosis model and in human IPF patients.
  • CTGF expression increased in vascular smooth muscle cells and endothelial cells during fibrogenesis.
  • Recombinant CTGF synergized with TGF-β to enhance profibrotic markers in fibroblasts.
  • Pamrevlumab partially attenuated fibrosis in the rat model, indicating CTGF's crucial role.

Conclusions:

  • CTGF is upregulated in both experimental and human pulmonary fibrosis, playing a key role in fibrogenesis.
  • Both profibrotic mediators and the fibrotic microenvironment contribute to sustained CTGF upregulation.
  • CTGF inhibition, exemplified by pamrevlumab, presents a promising therapeutic strategy for pulmonary fibrosis.