FGF10 and chronic obstructive pulmonary disease: In line with previous reports, our findings suggest that FGF10 inhibits the CSE-induced endothelial apoptosis mainly through FGFR1 signaling as (1) database analysis revealed that FGFR1, but not FGFR2, is suppressed during COPD, (2) FGFR1, but not FGFR2, is the predominant FGFR expressed in pulmonary endothelial cells, and (3) FGF10 serves as a ligand binding to FGFR1b, though with a relative low affinity compared to FGFR2b [19, 43].