Capacity of astrocytes to promote axon growth in the injured mammalian central nervous system

Matin Hemati-Gourabi, Tuoxin Cao, Megan K. Romprey, Meifan Chen

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations


Understanding the regulation of axon growth after injury to the adult central nervous system (CNS) is crucial to improve neural repair. Following acute focal CNS injury, astrocytes are one cellular component of the scar tissue at the primary lesion that is traditionally associated with inhibition of axon regeneration. Advances in genetic models and experimental approaches have broadened knowledge of the capacity of astrocytes to facilitate injury-induced axon growth. This review summarizes findings that support a positive role of astrocytes in axon regeneration and axon sprouting in the mature mammalian CNS, along with potential underlying mechanisms. It is important to recognize that astrocytic functions, including modulation of axon growth, are context-dependent. Evidence suggests that the local injury environment, neuron-intrinsic regenerative potential, and astrocytes’ reactive states determine the astrocytic capacity to support axon growth. An integrated understanding of these factors will optimize therapeutic potential of astrocyte-targeted strategies for neural repair.

Original languageEnglish
Article number955598
JournalFrontiers in Neuroscience
StatePublished - Sep 20 2022

Bibliographical note

Funding Information:
Research in the authors’ laboratory was supported by grants from NIH/NINDS (R01NS121193), American Heart Association (18CDA34060059), Kentucky Spinal Cord and Head Injury Research Trust training fund, and University of Kentucky CCTS pilot award from NIH/NCATS (UL1TR001998).

Publisher Copyright:
Copyright © 2022 Hemati-Gourabi, Cao, Romprey and Chen.


  • CNS injury
  • astrogliosis
  • axon regeneration
  • axon sprouting
  • glial scar
  • neural repair
  • reactive astrocytes
  • spinal cord injury

ASJC Scopus subject areas

  • Neuroscience (all)


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