SARM1 promotes neuroinflammation and inhibits neural regeneration after spinal cord injury through NF-κB signaling

Spinal cord injury (SCI) can lead to permanent paralysis due to a primary injury followed by secondary injury events like inflammation and cell death. Axonal degeneration, where nerve fibers break down, is a key feature of SCI. The protein SARM1 has been identified as a key mediator of Wallerian degeneration (WD), a programmed self-destruction process that promotes axon breakdown. However, its specific functions after SCI are not well understood. This study found that SARM1 is upregulated in neurons and astrocytes after SCI. Deleting SARM1 in these cells promoted nerve regeneration and reduced inflammation, suggesting that inhibiting SARM1 could be a potential treatment for SCI.

• 1
  SARM1 was upregulated in neurons and astrocytes at the early stage after SCI.
• 2
  Conditional deletion of SARM1 in neurons and astrocytes promoted the functional recovery of behavior performance after SCI.
• 3
  Conditional deletion of SARM1 in neurons and astrocytes reduced neuroinflammation by downregulating NF-κB signaling through upregulation of HSP70 after SCI.