Traumatic optic neuropathy (TON) is commonly associated with blunt ocular trauma and craniofacial injuries, leading irreversible visual impairment.Like other mammalian mature central nerve system (CNS) neurons, retinal ganglion cell (RGC) is normally unable to regenerate axon spontaneously after optic nerve injury.The failure of axon regeneration has been attributed to the apoptosis of RGC, loss of intrinsic growth capacity of mature neurons, lack of suitable stimuli, and inhibition of extracellular environment.Via activating the intrinsic growth capacity of mature RGC, overcoming the inhibitory extracellular environment of damaged optic nerve, and providing appropriate inflammatory stimuli to initiate the regeneration process, mature RGC can be transformed into an active regenerative state allowing these neurons to survive axotomy and to regenerate axons in the injured optic nerve.Moreover, exploiting gene therapy based on adeno-associated virus may be a promising translatable treatment strategy for TON.

Traumatic optic neuropathy; Neuroregeneration; Adeno-associated virus; Gene therapy