Aryl hydrocarbon receptor restricts axon regeneration of DRG neurons in response to injury

Injured nerve cells must balance protecting themselves with regrowing damaged axons. This study identifies a protein, the aryl hydrocarbon receptor (AhR), as a key regulator that favors self-protection over axon regeneration. Blocking AhR could potentially help nerves repair themselves more effectively. The aryl hydrocarbon receptor (AhR) senses environmental cues and adjusts cell behavior. In nerve cells, AhR activation inhibits axon regeneration. Removing AhR in mice accelerates nerve regrowth after injury. AhR affects inflammation and growth-related pathways after nerve damage. The study also found signaling interactions between AhR and HIF-1α, another protein involved in cellular responses to low oxygen levels. The growth benefits of removing AhR require HIF-1α. These findings offer insights into how to improve nerve repair strategies by targeting AhR.

• 1
  AhR activation in DRG neurons inhibits axon regeneration after nerve injury.
• 2
  Conditional deletion of Ahr in neurons promotes axon regeneration and functional recovery after sciatic nerve injury.
• 3
  The growth-promoting effect of AhR ablation is dependent on HIF-1α, suggesting a collaborative relationship between these transcription factors.