A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis promotes epithelial metaplasia in idiopathic pulmonary fibrosis. This study investigates the role of TGF-β1 signaling in idiopathic pulmonary fibrosis (IPF) and its interaction with epithelial cells. Researchers found that fibroblast-specific inhibition of TGF-β1 signaling using epigallocatechin gallate (EGCG) reduces profibrotic signaling and epithelial metaplasia in IPF. They identified sFRP2 as a TGF-β1-induced gene in fibroblasts that promotes epithelial metaplasia by activating a noncanonical Wnt signaling pathway. The study shows that TGF-β1 signaling in fibroblasts promotes a basaloid state in alveolar epithelial cells (AEC2s), which is then regulated by sFRP2 to activate a mature basal cell program. This process is mediated by the Wnt receptor Frizzled 5 (Fzd5) and downstream calcineurin signaling, leading to nuclear accumulation of NFATc3 and expression of KRT5. These findings highlight the role of TGF-β1 signaling in IPF and suggest that EGCG could be a potential therapeutic agent for reducing IPF-related transcriptional changes. The study also identifies sFRP2 as a key mediator of dysfunctional epithelial signaling in IPF. The results provide insights into the molecular mechanisms underlying IPF and suggest that targeting TGF-β1 signaling could be a promising therapeutic approach.A fibroblast-dependent TGF-β1/sFRP2 noncanonical Wnt signaling axis promotes epithelial metaplasia in idiopathic pulmonary fibrosis. This study investigates the role of TGF-β1 signaling in idiopathic pulmonary fibrosis (IPF) and its interaction with epithelial cells. Researchers found that fibroblast-specific inhibition of TGF-β1 signaling using epigallocatechin gallate (EGCG) reduces profibrotic signaling and epithelial metaplasia in IPF. They identified sFRP2 as a TGF-β1-induced gene in fibroblasts that promotes epithelial metaplasia by activating a noncanonical Wnt signaling pathway. The study shows that TGF-β1 signaling in fibroblasts promotes a basaloid state in alveolar epithelial cells (AEC2s), which is then regulated by sFRP2 to activate a mature basal cell program. This process is mediated by the Wnt receptor Frizzled 5 (Fzd5) and downstream calcineurin signaling, leading to nuclear accumulation of NFATc3 and expression of KRT5. These findings highlight the role of TGF-β1 signaling in IPF and suggest that EGCG could be a potential therapeutic agent for reducing IPF-related transcriptional changes. The study also identifies sFRP2 as a key mediator of dysfunctional epithelial signaling in IPF. The results provide insights into the molecular mechanisms underlying IPF and suggest that targeting TGF-β1 signaling could be a promising therapeutic approach.