In animal models, it was revealed that the overexpression of transforming growth factor β1 (TGF-β1), a pivotal regulator of pulmonary fibrosis, would result in the suppression of SP-A, SP-B, and SP-C expression, thereby impairing pulmonary surfactant synthesis and leading to elevated surface tension [62,63]. Here, TGFB1 is linked to pulmonary fibrosis.