中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (3): 491-492.doi: 10.4103/1673-5374.380894

• 观点:脊髓损伤修复保护与再生 • 上一篇    下一篇

细胞外囊泡在脊髓损伤后神经再生中的作用

  

  • 出版日期:2024-03-15 发布日期:2023-09-01

Extracellular vesicles for neural regeneration after spinal cord injury

Young-Ju Lim, Wook-Tae Park, Gun Woo Lee*#br#   

  1. Department of Orthopedic Surgery, Yeungnam University Medical Center, Yeungnam University College of Medicine, Daegu, Korea
  • Online:2024-03-15 Published:2023-09-01
  • Contact: Gun Woo Lee, MD, PhD, gwlee1871@gmail.com.
  • Supported by:
    This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (No. 2022R1C1C1005410) (to GWL).

摘要: https://orcid.org/0000-0002-8441-0802 (Gun Woo Lee)

Abstract: What is spinal cord injury: Spinal cord injury (SCI) is the damage to the structure of the bundles of cells and nerves that communicate signals from the brain to the body and extremities. The pathology of SCI includes both primary and secondary injuries (Morales et al., 2016). Physical forces such as compression, shearing, contusion, and tearing are major causes of primary injury in SCI. There are two main processes in primary injury: acute and subacute. The acute phase includes traumatic disruption of axons and hemorrhage of the blood vessels around the spinal cord. Hemorrhagic injury to the vessels can lead to increased edema within the neural and cord tissues, susceptibility to infiltration by microglia and astrocytes, excitotoxicity, and demyelination. Similarly, disruption of the blood-spinal cord barrier results in the release of inflammatory cytokines from specific cells and vessels. Primary injuries are surgically addressed by surgical decompression and stabilization. Meanwhile, secondary injuries are more complex than primary injuries, and no effective treatment for secondary injuries following SCI has been developed to date. The secondary injury involves several patho-mechanisms that seriously affect neural cells, the extracellular matrix within the spinal cord, and the surrounding structures. Among the injury processes, the activity of excitatory toxicity is a main cause for neural cell damage. The activity has been induced by the increased concentration of glutamate and glutamate receptors induce calcium channel permeability, resulting in an abnormal inflow of calcium ions. Guanosine triphosphate-binding protein-coupled metabotropic glutamate receptors induce inositol trisphosphate and release calcium ions from the endoplasmic reticulum. Previous studies have documented the protective role of glutamate receptor or calcium channel antagonists in neural cells. Whilst, the transmission of radicals, production of free radicals, and release of toxic and excitatory amino acids at the injured site are usually involved in the delayed phase of SCI. Specific proinflammatory cytokines, such as interleukin (IL)-1, IL-6, and tumor necrosis factor-α, may initially induce the differentiation of neural stem and progenitor cells to astrocytes. Similarly, cytokines are associated with tissue necrosis, the formation of a cavity of injury, and scarring at the injured area, resulting in the disruption of the healing process after SCI.