Evidence that metformin promotes fibrosis resolution via activating alveolar epithelial stem cells and FGFR2b signaling

Idiopathic pulmonary fibrosis (IPF) is a progressive disease lacking effective therapy. Metformin, an antidiabetic medication, has shown promising therapeutic properties in preclinical fibrosis models; however, its precise cellular targets and associated mechanisms in fibrosis resolution remain incompletely defined. Most research on metformin's effects has focused on mesenchymal and inflammatory responses with limited attention to epithelial cells. In this study, we utilized Sftpc lineage-traced and Fgfr2b conditional knockout mice, along with BMP2/PPAR

  • Lv, Y.
  • Zhang, Y.
  • Guo, X.
  • He, B.
  • Xu, H.
  • Xu, M.
  • Zou, L.
  • Lyu, H.
  • Wu, J.
  • Zeng, P.
  • Bellusci, S.
  • Jin, X.
  • Chen, C.
  • Cho, Y. C.
  • Li, X.
  • Zhang, J. S.

Keywords

  • Ampk
  • Alveolar stem cell
  • FGFR2b
  • Injury-activated alveolar progenitor
  • Metformin
  • Pulmonary fibrosis
  • Transgenic mice
Publication details
DOI: 10.1016/j.apsb.2025.07.023
Journal: Acta Pharm Sin B
Pages: 4711-4729
Number: 9
Work Type: Original
Access number: 41049730
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