TGFB1 and idiopathic pulmonary fibrosis: They showed that both TGF-β-activated fibroblasts and IPF fibroblasts induce RAS activation in ATII cells, and this process is at least partially driven by the secreted protein acidic and rich in cysteine (SPARC), supporting the concept that aberrant bidirectional epithelial–mesenchymal crosstalk contributes to the development of a profibrogenic microenvironment, where a chronic wound-healing response leads to the development of lung fibrosis [44].