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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Semin Nephrol. 2012 May;32(3):244–252. doi: 10.1016/j.semnephrol.2012.04.003

Fig. 3. TGF-β-induced TAK1 signaling and profibrotic response.

Fig. 3

TGF-β1-induced TAK1 activation triggers downstream signaling pathways such as the MKK4-JNK, or the MKK3-p38 cascade, and promotes degradation of Ik-B, which in turn lead to the activation of transcription factors ATF-2, AP-1 and NF-kB, respectively, to regulate the expression of extracellular matrix proteins, including collagens and fibronectin, and inflammatory cytokines. In addition, TGF-β1-induced Smad activation is also indispensible for TGF-β1-induced type I collagen expression through the crosstalk with TAK1-MKK3-p38 signaling axis.