FGF9-induced changes in cellular redox status and HO-1 upregulation are FGFR-dependent and proceed through both ERK and AKT to induce CREB and Nrf2 activation

- FGF9-induced HO-1 and γ-GCS expression was prevented by an FGFR inhibitor, PD173014.
- FGF9 induced ERK and AKT phosphorylation and CREB and Nrf2 activation in neurons.
- ERK or AKT inhibition prevented FGF9 antioxidative functions and neuroprotection.
- Knockdown of CREB or Nrf2 blocked FGF9 functions, but not ERK and AKT activity.
- FGF9-induced HO-1 and γ-GCS upregulation is mediated by the FGFR/ERK, AKT/CREB and Nrf2 signaling pathway.