Altogether, these data demonstrate that LOX is a downstream target of YAP-TEAD signaling in fibrotic AT2 cells and indicate that the fibrotic alveolar epithelium via active YAP-TEAD signaling and LOX secretion into the extracellular environment may contribute to extracellular collagen network formation in pulmonary fibrosis. This evidence concerns the gene LOX and pulmonary fibrosis.