Therapeutic Potential of Wnt-3a in Neurological Recovery after Spinal Cord Injury

Eur Neurol. 2019;81(3-4):197-204. doi: 10.1159/000502004. Epub 2019 Jul 23.


Background: Spinal cord injury (SCI) is a constant challenge in medical research and a global therapeutic problem. Treatment of this condition remains difficult in clinical practice. Hence, prevention, treatment, and rehabilitation of SCI have become imminent tasks in the medical field.

Summary: Recent evidence suggest the important role of Wnt/β-catenin signaling pathway, a canonical Wnt signaling pathway, in neural development, axon guidance, neuropathic pain relief, and neuronal survival. Wnt-3a is regarded as an activator of the canonical Wnt signaling pathway. This activator is expressed in the dorsal midline region and is responsible for spinal cord development. In addition, Wnt-3a plays a regulatory role in autophagy, apoptosis, and regeneration of neurons; neurogenic inflammation; and axon regeneration. Herein, we demonstrated that neuronal autophagy was regulated by Wnt-3a via β-catenin and mammalian target of rapamycin signaling pathways after SCI. Our study also discovered that the Wnt-3a provided a favorable microenvironment for the recovery of nerve function after SCI. Key Messages: This study systematically elaborates the neuroprotective effect of Wnt-3a and its neuroprotection molecular mechanism after SCI. This study provides a new molecular mechanism and research basis for clinical treatment of SCI.

Keywords: Apoptosis; Autophagy; Axon regeneration; Mammalian target of rapamycin signaling pathway; Neuroprotection; Spinal cord injury; Wnt-3a; Wnt/β-catenin signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Axons
  • Humans
  • Nerve Regeneration / physiology*
  • Neuroprotection / physiology*
  • Rats
  • Recovery of Function / physiology*
  • Spinal Cord / physiopathology
  • Spinal Cord Injuries / physiopathology*
  • Wnt Signaling Pathway / physiology*