Fig. (5) Anti-TGF-β-induced profibrotic effects of PPAR-γ ligands. TGF-β induces cell proliferation, migration, fibroblast activation, and mesenchymal transition from epithelial cells, endothelial cells, and adipocytes. All these processes contribute to fibrosis formation and progression. PPAR-γ ligands have been shown to inhibit these processes in a variety of cell types. And there is reciprocal regulation between TGF-β signaling and PPAR-γ axis. TGF-β suppresses PPAR-γ expression, which might contribute to persistent activation of TGF-β signaling; PPAR-γ ligands, through PPAR-γ-dependent and –independent mechanism, abrogate TGF-β signaling and might have therapeutic potential in fibrosis.