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. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: Kidney Int. 2015 Jan 7;87(5):948–962. doi: 10.1038/ki.2014.386

Figure 9.

Figure 9

Schematic reorientation of how loss of p47phox ameliorates the fibrotic response in integrin α1KO cells or mice. (A) Loss of integrin α1β1 leads to increased activation of EGFR (1) which in turn promotes p47phox membrane translocation and the assembly of the NADPH oxidase system by activating Rac1 (2) and/or ERK (3). NADPH-generated superoxide (4) can then exert a pro-fibrotic action by promoting collagen synthesis (5) and prolonging EGFR activation (6). (B) Loss of p47phox reduces this fibrotic response by dampening ROS production (4), collagen synthesis (5), and EGFR activation (6).