Neural Regeneration Research, 2017 · DOI: 10.4103/1673-5374.221144 · Published: December 1, 2017
Following CNS lesions, naïve astrocytes are converted into reactive astrocytes and eventually into scar-forming astrocytes that block axon regeneration and neural repair. Recent use of various genetic tools has made tremendous progress in better understanding genesis of reactive astrogliosis. The interactions between upregulated type I collagen and its receptor integrin β1 and the N-cadherin-mediated cell adhesion appear to play major roles for local astrogliosis around the lesion.
Targeting specific molecular and cellular changes at a given stage of astrogliosis after CNS injury can lead to effective therapies.
Intervening in the transformation of reactive astrocytes to scar-forming astrocytes can help injured axons grow and potentially improve functional recovery.
Administering anti-β1 antibody or N-cadherin antibody can decrease astrocytic scar formation and improve behavioral recovery in mice with SCI.