Mitochondrial dysfunction as a target in spinal cord injury: intimate correlation between pathological processes and therapeutic approaches

Traumatic spinal cord injuries (SCI) interrupt the connection of axonal projections, leading to alterations in locomotor, sensory, and autonomic functions. Mitochondrial dysfunction during the secondary stage of SCI reduces adenosine triphosphate levels, leading to calcium overload, reactive oxygen species formation, and excitotoxicity. Restoring mitochondrial function early in the secondary injury stage could be a potentially effective therapeutic intervention to overcome motor and sensory failure after SCI.

• 1
  Mitochondrial dysfunction is intimately linked with axonal regeneration failure in the context of spinal cord injury.
• 2
  Mitochondria-targeted therapeutical approaches, such as antioxidant molecules, removing mitochondrial anchor proteins, and increasing energetic metabolism through creatine treatment, may enhance functional recovery.
• 3
  Proper crosstalk between ATP formation and a decrease in ROS levels is necessary to promote neuronal repair.