Western blot showing that TGF-β1 stimulation resulted in the activation of canonical TGF-β-Smad2/3 signaling, assessed by the elevated p-Smad2 and p-Smad3 (Figures 5A–C), followed by the expression of downstream transcription factors Snail and Slug (Figures 5A, D, E), key regulators that mediated TGF-β-Smad signaling triggered the overexpression and excessive production of ECM proteins in pulmonary fibrosis. Here, SMAD3 is linked to pulmonary fibrosis.