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. 2022 Mar 28;18(7):2795–2806. doi: 10.7150/ijbs.71595

Figure 1.

Figure 1

Smad3 signaling and crosstalk pathways in renal fibrosis. After binding to TβRII, TGF-β1 activates the TβRI-kinase which phosphorylates Smad3. The phosphorylated Smad3 translocates into the nucleus and regulates the target gene transcription. Smad7 is an inhibitory Smad that functions to block Smad3 activation by degrading the TβRI and preventing phosphorylation of Smad3.Ang II, AGEs and CRP can activate TGF-β1-independent signaling via the ERK/p38/ MAPK crosstalk pathway. Red arrows/ symbols represent pathogenic or positive regulation pathway, while blue lines/ symbols indicate protective or negative regulation pathways in fibrosis.