Figure 2 Crosstalk between TGF-β/Smad and other pathways in tissue fibrosis Figure 2 | Crosstalk between TGF-β/Smad and other pathways in tissue fibrosis.

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Figure 2 Crosstalk between TGF-β/Smad and other pathways in tissue fibrosis Figure 2 | Crosstalk between TGF-β/Smad and other pathways in tissue fibrosis. In addition to regulating transcription by phosphorylating Smad2 and Smad3 and facilitating formation of a Smad2/3/4 complex that induces transcription, TGF-β1 interacts with other signalling pathways. It can activate the mitogen-activated protein kinases (MAPKs), p38, JNK and ERK in a Smad-independent manner. MAPKs can phosphorylate the linker region of Smad proteins to modulate Smad3 transcriptional activity. In addition, other signalling pathways can activate MAPKs (for example, angiotensin II, oxidative stress, hyperglycaemia) and thereby modify Smad phosphorylation. Wnt ligand-induced β-catenin stabilization can enable β-catenin to complex with Smad proteins and enhance gene transcription of profibrotic molecules. Mammalian target of rapamycin complex 1 (mTORC1) has a poorly defined role in facilitating the induction of reactive oxygen species (ROS), hypoxia-responsive element activity and hypoxia-inducible factor-1α expression by TGF-β/Smad. The p53 tumour suppressor can be induced by TGF-β and can form complexes with Smad2/3 to regulate gene transcription. TGF-β can also transactivate the epidermal growth factor receptor (EGFR) via a ROS-dependent mechanism. Bone morphogenic protein-7 (BMP-7) activates Smad1 and Smad5, which are negative regulators of Smad3-based gene transcription. Meng, X.-m. et al. (2016) TGF-β: the master regulator of fibrosis Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.48