COL1A1 and idiopathic pulmonary fibrosis: Though IPF lung fibroblasts responded to heparin + FGF1 treatment by attenuating COL1a1 expression and increased apoptosis, increased p-ERK1/2 signaling along with enhanced cell migration was also observed reflecting a potentially dual nature of FGF1/FGFR in the context of lung fibrosis.