Abstract:

Central nervous system (CNS) injuries remain a leading cause of functional disabilities worldwide, often resulting in permanent neurological impairments, due to the inability to repair and regenerate damaged connections. A major contributing factor to this loss of regenerative capacity is the formation of glial scar tissue (Cregg et al., 2014), traditionally regarded as a potent mechanical and molecular barrier to repair. The glial scar comprises primarily reactive astrocytes, a subset of NG2 glia, inflammatory cells and extracellular matrix (ECM) glycoproteins – mainly chondroitin sulfate proteoglycans (CSPG; Cregg et al., 2014). The transition of astrocytes into their reactive state, as a consequence of pathological insults to the CNS, including trauma, inflammation and strokes, is characterized by changes in their morphology, gene/protein expression and role.These features are regulated by a host of intrinsic and extrinsic factors that modulate astrocyte reactivity, behaviour, proliferation and ECM secretions, ultimately culminating in the formation of the glial scar (Sofroniew, 2009). While astrogliosis and glial scarring have been well studied, especially in the context of repair inhibition,new evidence has begun to shed light on the previously unspecified neuroprotective role of reactive astrocytes after injury. Therefore,this perspective will discuss the most recent and significant research that has had altered the once held view of the astrocyte being solely inhibitory to repair following CNS injury.