SMAD2 and fibrosis: Similarly, PRP can also significantly inhibit the up regulation of fibrosis related proteins induced by PTJC in vivo. These results suggest that PRP can attenuate pathological changes of joint capsule fibrosis during PTJC, which may be implemented by inhibiting TGF-β1/Smad2/3 signaling and downstream fibrotic marker expression in joint capsule fibroblasts.