Neural Regen Res, 2018 · DOI: 10.4103/1673-5374.235226 · Published: August 1, 2018
The glial scar, traditionally viewed as a barrier to axon regeneration after spinal cord injury (SCI), is now understood as a complex, multicellular structure. It limits the expansion of inflammatory processes shortly following SCI and persists chronically to limit axon regeneration. Reactive astrocytes, a key component of the glial scar, respond to inflammation by changing their morphology and producing pro-inflammatory factors, creating an inhibitory environment for axonal regeneration. This is in contrast to organisms like zebrafish, which exhibit limited inflammatory responses and scar formation after injury. The glial scar's fibrotic components, including collagen type I, also contribute to inhibiting axon outgrowth. While the scar helps stabilize inflammation early after injury, its chronic persistence hinders axon regeneration and functional recovery.
Future SCI treatments should consider the specific roles of different cell types and molecules within the glial scar, rather than simply trying to remove the scar entirely.
Timing is crucial in SCI treatment; intervening too early or too late can have different effects on inflammation, axon regeneration, and functional recovery.
Given the complexity of CSPG expression and sulphation, personalized treatment strategies may be necessary to address the specific molecular environment of each patient's injury.