FANCC deficiency mediates microglial pyroptosis and secondary neuronal apoptosis in spinal cord contusion

Spinal cord injury (SCI) can lead to paralysis and neurological issues. Microglial pyroptosis, a form of cell death, contributes to neuroinflammation after SCI. The study investigates the role of FANCC in regulating this process. FANCC, known for its anti-inflammatory effects, is examined for its potential to control microglial pyroptosis. The research explores how FANCC influences neuroinflammation in SCI mice. The study found that FANCC deficiency leads to microglia pyroptosis, neuronal apoptosis, and neurological damage after SCI. FANCC regulates the p38/NLRP3 pathway, affecting the inflammatory response.

• 1
  Overexpression of FANCC suppressed microglial pyroptosis by inhibiting p38/NLRP3 expression, which in turn reduced neuronal apoptosis.
• 2
  Knockdown of FANCC increased the degree of neuronal apoptosis by aggravating microglial pyroptosis.
• 3
  FANCC deficiency led to increased glial scar formation, severe myelin sheath destruction, poor axon outgrowth and reduced locomotor function recovery.