Idiopathic pulmonary fibrosis (IPF) is a progressive clinical syndrome of fatal outcome. The
lack of information about the signaling pathways that sustain fibrosis and the myofibroblast
phenotype has prevented the development of targeted therapies for IPF. Our previous study
showed that isolated fibrogenic lung fibroblasts have high endogenous levels of the
hyaluronan receptor, CD44V6 (CD44 variant containing exon 6), which enhances the
TGFβ1 autocrine signaling and induces fibroblasts to transdifferentiate into myofibroblasts …