TGFBR2 and pulmonary fibrosis: To investigate whether DST-3 influences pulmonary fibrosis through TGF/Smad, in the presence or absence of TGF−β1, we found that the protein levels of transforming growth factor-β receptor type I (TGF-β RI) and transforming growth factor-beta receptor type II (TGF-β RII) were significantly upregulated (Figure 5A), and DST-3 reversed this upregulation in the presence of TGF-β1 for 48 h (Figure 5B).