Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury

Mol Neurobiol. 2023 Nov;60(11):6556-6565. doi: 10.1007/s12035-023-03494-6. Epub 2023 Jul 17.

Abstract

Mitochondria are important organelle of eukaryotic cells. They consists of a large number of different proteins that provide most of the ATP and supply power for the growth, function, and regeneration of neurons. Therefore, smitochondrial transport ensures that adequate ATP is supplied for metabolic activities. Spinal cord injury (SCI), a detrimental condition, has high morbidity and mortality rates. Currently, the available treatments only provide symptomatic relief for long-term disabilities. Studies have implicated mitochondrial transport as a critical factor in axonal regeneration. Hence, enhancing mitochondrial transports could be beneficial for ameliorating SCI. Syntaphilin (Snph) is a mitochondrial docking protein that acts as a "static anchor," and its inhibition enhances mitochondrial transports. Therefore, Snph as a key mediator of mitochondrial transports, may contribute to improving axonal regeneration following SCI. Herein, we examine Snph's biological effects and its relation to mitochondrial pathway. Then, we elaborate on mitochondrial transports after SCI, the possible role of Snph in SCI, and some possible therapeutic approaches by Snph.

Keywords: Akt-PAK5 signaling; Axon regeneration; Mitochondrial transport; P21 activated kinase 5 (PAK5); Spinal cord injury (SCI); Syntaphilin (Snph).

Publication types

  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Axonal Transport
  • Axons* / metabolism
  • Humans
  • Microtubule-Associated Proteins / metabolism
  • Mitochondria / metabolism
  • Nerve Regeneration
  • Spinal Cord / metabolism
  • Spinal Cord Injuries* / metabolism

Substances

  • Microtubule-Associated Proteins
  • Adenosine Triphosphate