SIS3, a specific inhibitor of smad3, attenuates bleomycin-induced pulmonary fibrosis in mice

Juanjuan Shou, Jingjing Cao, Shanshan Zhang, Ruicong Sun, Mengmeng Zhao, Keqiang Chen, Shao Bo Su, Jianhua Yang, Tianshu Yang

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Pulmonary fibrosis (PF) is a fatal respiratory disease with no effective medical treatments available. TGF-β/Smads signaling has been implicated to play an essential in the pathogenesis of PF, in which Smad3 act as the integrator of pro-fibrosis signals. In this study, we determined the effect of SIS3, a specific inhibitor of Smad3, in an experimental mouse model of lung fibrosis. We observed that SIS3 treatment significantly reduced bleomycin (BLM)-induced pathological changes and collagen deposition in the lung as indicated by Masson staining, real-time PCR and hydroxyproline content assay. As expected, the levels of Smad3 phosphorylation were decreased in the lung of mice treated with SIS3. Furthermore, SIS3 treatment also suppressed BLM-induced infiltration of inflammatory cells in the lung. Taken together, our results suggest that SIS3 ameliorated BLM-induced PF in mouse lungs. Thus, targeting Smad3 with SIS3 may be an effective approach for treatment of fibrotic disorders.

Original languageEnglish (US)
Pages (from-to)757-762
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Sep 5 2018


  • Inflammation
  • Pulmonary fibrosis
  • Smad3
  • Transforming growth factor beta

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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