中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (5): 951-952.doi: 10.4103/1673-5374.382247

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

自噬在颅脑损伤后神经炎症中的作用

  

  • 出版日期:2024-05-15 发布日期:2023-10-31

Autophagy in neuroinflammation after traumatic brain injury

Chinmoy Sarkar*, Marta M. Lipinski*   

  1. Shock, Trauma and Anesthesiology Research (STAR) Center, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD, USA (Sarkar C, Lipinski MM)
    Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, USA (Lipinski MM)
  • Online:2024-05-15 Published:2023-10-31
  • Contact: Marta M. Lipinski, PhD, mlipinski@som.umaryland.edu; Chinmoy Sarkar, PhD, csarkar@som.umaryland.edu.
  • Supported by:
    This work was supported by NIH funding (R01NS091218 and R01NS115876) to MML.

摘要: https://orcid.org/0000-0002-7537-9014 (Marta M. Lipinski) 
https://orcid.org/0000-0001-5508-8968 (Chinmoy Sarkar)

Abstract: Traumatic brain injury (TBI) is an acquired injury of the brain caused by the impact of external forces on the brain (Maas et al., 2008). It is a major cause of death and disability among people of all ages (Maas et al., 2008). The primary mechanical injury to the brain initiates a cascade of secondary biochemical events that lead to acute and chronic neurodegeneration and activation of inflammatory pathways (Maas et al., 2008). Both brain-resident microglia and blood-derived myeloid cells – macrophages and monocytes that infiltrate the brain due to injury-induced blood-brain barrier damage, contribute to the inflammatory responses after TBI (Morganti et al., 2015). These cells are responsible for clearing the damaged tissue through phagocytosis (Henry et al., 2020). This, in turn, activates the inflammasome and interferon type-1-mediated innate immune responses (Henry et al., 2020). The initial inflammatory response is important for resolving any tissue damage as it can remove the damaged cells and clear the injured area for regeneration (Henry et al., 2020). However, this is contingent on efficient degradation of phagocytosed dead cells and tissue debris by the immune cells, and their eventual transition to anti-inflammatory states to promote tissue regeneration. In TBI, neuroinflammation persists chronically and contributes to long-term pathology and poor recovery.