SMAD2 and pulmonary fibrosis: These results revealed that CB1R activation, which acted as a negative regulation of canonical TGF-β-Smad2/3 signaling, downregulated TGF-β-triggered overexpression of ECM proteins in lung fibroblasts, but did not affect normal ECM production, and CB1R agonist was proven useful as a potential therapeutic option for pulmonary fibrosis.