Fig. 8.

Macrophage GIT1 is critical to successful bone regeneration via regulating inflammatory responses in an ERK/NRF2‐dependent way. In response to LPS, once GIT1 is involved, it promotes NRF2 to stabilize and translocate into the nucleus for genes transcriptionally regulation via phosphorylating ERK. In the absence of GIT1, inactivated ERK/NRF2 axis could lead to abnormal upregulation of ROS production and IL1β secretion and glycolysis, which is detrimental to the osteogenic differentiation of BMSCs. Furthermore, macrophage GIT1‐mediated activation of ERK/NRF2 controls glycolysis by limiting PFKFB3 expression.