CX3CL1-mediated neuronal "rescue signal" influences inflammation progression following spinal cord injury via microglia.

Spinal cord injury (SCI) is a refractory diseases that leads to lasting impairments in sensory and motor functions. Following nerve injury, CX3CL1, a neuron membrane protein, is released. Research suggests that CX3CL1 neurons possess a unique signaling mechanism for rescue. The objective of this study was to investigate the neuroprotective mechanism of CX3CL1 after spinal cord injury. Our findings indicate that injured neurons release CX3CL1, which binds to microglia and activates the NF-κB pathway. This activation downregulates IKB and P65 phosphorylation, thereby controlling the progression of inflammation after spinal cord injury. Consequently, more neurons are protected, leading to the restoration of nerve function. In conclusion, this study has discovered that CX3CL1 played a critical role in neuroprotection following spinal cord injury, making it a potential therapeutic target for treating this condition.