摘要Traumatic injuries to the central nervous system(CNS)result in disruption of the intricate network of axons which connect functionally related neurons that are widely distributed throughout the brain and spinal cord.Under normal conditions,maintenance of this complex system is structurally and functionally supported by astrocytes(ACs)and other glial cells,the processes of which form a framework surrounding neuronal cell bodies,dendrites,axons,and synapses.Following injury,however,ACs adopt a reactive,scar-forming phenotype to establish a barrier that limits the spread of inflammatory cells and molecules from the primary lesion site to adjacent nervous tissue,effectively limiting secondary tissue degeneration.Unfortunately,due to the persistent nature of the resulting glial scar,this initially protective function acts as a double-edged sword as it also suppresses CNS axon sprouting and regeneration across the lesion site,resulting in permanent disability for those affected.