Figure 5.

Many processes which contribute to fibrotic disease are mediated by Smad3. These include: (1) epithelial to mesenchymal transdifferentiation (EMT) which is important in the induction of renal interstitial fibrosis and proliferative vitreoretinopathy (PVR); (2) recruitment of inflammatory cells and fibroblasts and autoinduction of transforming growth factor-β (TGF-β) in these cells which is involved in induction of radiation-induced fibrosis and pulmonary fibrosis and (3) induction of collagen synthesis by TGF-β. Inhibitors of Smad3 could act at multiple sites to inhibit fibrosis.