Skip to main content


Fig. 2 | Cell & Bioscience

Fig. 2

From: TGF-β in fibrosis by acting as a conductor for contractile properties of myofibroblasts

Fig. 2

TGF-β1 effects on the balance between the canonical WNT/β-catenin pathway and PPARγ. WNT activation inhibits the β-catenin destruction complex, which results in the β-catenin accumulation in the cytosol and then its translocation to the nucleus for activating WNT target genes. Following WNT stimulation, TAZ inhibits the phosphorylation of DSH and dissociates it from the β-catenin destruction complex. The destruction complex is inhibited because YAP and TAZ dissociate from the complex. Following TGF-β stimulation, AXIN promotes the tail-phosphorylation of Smad2/3. The activated Smad2/3-Smad4 complex associates with TAZ and YAP and then translocates to the nucleus for activation of Smad targets. TGF-β1 induces Smad2/3 and PI3K/AKT pathway activation. PPARγ inhibits β-catenin/TCF-LEF-induced activation of the WNT target genes. TGF-β also enhances WNT signaling through inhibition of DKK1. PPARγ actives DKK1 and inactivates PI3K/AKT. APC adenomatous polyposis, DKK1 Dickkopf-1, DSH disheveled, FZD frizzled, GSK-3β glycogen synthase kinase-3β, LRP5/6 protein 5/6 connected to the low-density lipoprotein receptor, PPARγ peroxisome proliferator-activated receptor gamma, TCF/LEF T cell factor/lymphoid enhancer factor, TGF transforming growth factor

Back to article page