中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (4): 973-989.doi: 10.4103/NRR.NRR-D-23-02091

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

创伤性脑损伤中的星形胶质细胞、反应性星形胶质形成和胶质瘢痕形成

  

  • 出版日期:2025-04-15 发布日期:2024-06-30

Astrocytes, reactive astrogliosis, and glial scar formation in traumatic brain injury

María Belén Cieri, Alberto Javier Ramos*   

  1. Laboratorio de Neuropatología Molecular, IBCN UBA-CONICET, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina
  • Online:2025-04-15 Published:2024-06-30
  • Contact: Alberto Javier Ramos, PhD, jramos@fmed.uba.ar.
  • Supported by:
    This work was supported by grants PICT 2019-0851; 2017-2203, UBACYT and PIP CONICET (to AJR).

摘要: https://orcid.org/0000-0003-4009-6337 (Alberto Javier Ramos)

Abstract: Traumatic brain injury is a global health crisis, causing significant death and disability worldwide. Neuroinflammation that follows traumatic brain injury has serious consequences for neuronal survival and cognitive impairments, with astrocytes involved in this response. Following traumatic brain injury, astrocytes rapidly become reactive, and astrogliosis propagates from the injury core to distant brain regions. Homeostatic astroglial proteins are downregulated near the traumatic brain injury core, while pro-inflammatory astroglial genes are overexpressed. This altered gene expression is considered a pathological remodeling of astrocytes that produces serious consequences for neuronal survival and cognitive recovery. In addition, glial scar formed by reactive astrocytes is initially necessary to limit immune cell infiltration, but in the long term impedes axonal reconnection and functional recovery. Current therapeutic strategies for traumatic brain injury are focused on preventing acute complications. Statins, cannabinoids, progesterone, beta-blockers, and cerebrolysin demonstrate neuroprotective benefits but most of them have not been studied in the context of astrocytes. In this review, we discuss the cell signaling pathways activated in reactive astrocytes following traumatic brain injury and we discuss some of the potential new strategies aimed to modulate astroglial responses in traumatic brain injury, especially using cell-targeted strategies with miRNAs or lncRNA, viral vectors, and repurposed drugs.

Key words: astrocyte, glial scar,  innate immunity,  neuroinflammation,  stab injury,  Toll-like receptors