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diopathic pulmonary fibrosis (IPF) is characterized by progressive (myo)fibroblast accumulation and collagen deposition. One possible source of (myo)fibroblasts is epithelial cells that undergo epithelial-mesenchymal transition (EMT), a process frequently mediated by TGF-β. In this issue of the JCI, Kim et al. report that epithelial cell–specific deletion of α3 integrin prevents EMT in mice, thereby protecting against bleomycin-induced fibrosis (see the related article beginning on page 213). The authors propose a novel mechanism linking TGF-β and β-catenin signaling in EMT through integrin-dependent association of tyrosine-phosphorylated β-catenin and pSmad2 and suggest targeted disruption of this interaction as a potential therapeutic approach.
