中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (8): 2304-2306.doi: 10.4103/NRR.NRR-D-24-00371

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

利用先进的微系统解读创伤性脑损伤中小胶质细胞的机械生物学

  

  • 出版日期:2025-08-15 发布日期:2024-12-13

Deciphering the mechanobiology of microglia in traumatic brain injury with advanced microsystems

Anthony Procès, Sylvain Gabriele*   

  1. Univ. Grenoble Alpes, Inserm, U1216, Grenoble Institut des Neurosciences, Grenoble, France (Procès A) Mechanobiology & Biomaterials Group, CIRMAP, Research Institute for Biosciences, University of Mons, Mons, Belgium (Gabriele S)
  • Online:2025-08-15 Published:2024-12-13
  • Contact: Sylvain Gabriele, PhD, sylvain.gabriele@umons.ac.be.
  • Supported by:
    SG acknowledges funding from FEDER Prostem Research Project, No. 1510614 (Wallonia DG06), the F.R.S.-FNRS Epiforce Project, No. T.0092.21, the F.R.S.-FNRS CellSqueezer Project, No. J.0061.23, the F.R.S.-FNRS Optopattern Project, No. U.NO26.22 and the Interreg MAT(T)ISSE Project, which is financially supported by Interreg France-WallonieVlaanderen (Fonds Européen de Développement Régional, FEDER-ERDF), Programme Wallon d’Investissement Région Wallone pour les instruments d’imagerie (INSTIMAG UMONS #1910169). AP acknowledges postdoctoral support from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (AdG grant agreement no. 834317, Fueling Transport, PI Frédéric Saudou).

摘要: https://orcid.org/0000-0002-4785-8931 (Anthony Procès) https://orcid.org/0000-0001-8696-8052 (Sylvain Gabriele

Abstract: Advanced microsystems in traumatic brain injury research: Traumatic brain injury (TBI) results from a mechanical insult to the brain, leading to neuronal and axonal damage and subsequently causing a secondary injury. Within minutes of TBI, a neuroinflammatory response is triggered, driven by intricate molecular and cellular inflammatory processes. The temporal progression of TBI events has been investigated using animal models, human surgical and post-mortem tissue samples, and the analysis of cerebrospinal fluid and plasma from TBI patients. However, the complex interplay between injured brain cells remains poorly understood. TBI induces immediate cell death at the site of impact (primary injury), which is dependent on the severity and depth of the injury. Damaged cells release damage-associated molecular patterns, which signal to resident and infiltrating immune cells via pattern recognition receptors. At the injury site, astrocytes, microglia, and damaged neurons secrete cytokines and chemokines, which activate microglia and astrocytes, and recruit peripheral immune cells that penetrate the compromised blood–brain barrier during the acute post-traumatic period (Nespoli et al., 2024). Consequently, TBI is a mechanobiological disorder characterized not only by the dysregulation of neuronal cells but also by a complex interplay of signaling pathways among brain cells.