SMAD2 and pulmonary fibrosis: These findings provided the first evidence that CB1R acted as a negative regulator for TGF-β1-Smad2/3 signaling and its associated fibroblast activation in pulmonary fibrosis (Figure 6), and thus, the overexpression of CB1R on fibroblasts might be a druggable target for the therapy of pulmonary fibrosis.