PDE4 inhibitor DC591017 ameliorates pulmonary fibrosis through modulating fibroblasts-epithelial cells-alternatively activated macrophages crosstalk - PubMed
4 hours ago
- #Pulmonary Fibrosis
- #PDE4 Inhibitor
- #Macrophage Polarization
- PDE4 inhibitor DC591017 shows potential in treating idiopathic pulmonary fibrosis (IPF) by modulating interactions between fibroblasts, epithelial cells, and macrophages.
- In a bleomycin-induced mouse model, DC591017 (10 mg/kg) reduced lung damage, collagen deposition, and improved lung function, comparable to nintedanib.
- Mechanistically, DC591017 inhibits fibroblast activation, epithelial-mesenchymal transition (EMT), and M2 macrophage polarization.
- Lung-on-a-chip models confirmed DC591017's role in regulating macrophages-fibroblasts-epithelial cells interactions to alleviate fibrosis.
- DC591017 emerges as a promising therapeutic candidate for IPF due to its multi-target anti-fibrotic effects.