TGFB1 and renal fibrosis: In vitro, Wnt3a, a molecule that promoted typical Wnt signaling pathway, exacerbated IL-4 or TGF-β1-induced macrophage M2 polarization as well as STAT3 phosphorylation and nuclear translocation; conversely, which in turn inhibited macrophage M2 polarization and suppressed the expression of the profibrotic cytokines PDGF, VEGF, TGF-β and connective tissue growth factor, thereby alleviating renal fibrosis (116).