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颅脑损伤中的星形胶质细胞:有好有坏。

Astrocytes in the Traumatic Brain Injury: the Good and the Bad.

机构信息

Institute of Neuroscience, Hengyang Medical College, University of South China, Hengyang, 421001, Hunan, China.

Beijing Institute of Basic Medical Sciences, 100850 Beijing, China; Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, Jiangsu, China; Chinese Institute for Brain Research (CIBR), 102206 Beijing, China.

出版信息

Exp Neurol. 2022 Feb;348:113943. doi: 10.1016/j.expneurol.2021.113943. Epub 2021 Dec 2.


DOI:10.1016/j.expneurol.2021.113943
PMID:34863998
Abstract

Astrocytes control many processes of the nervous system in health and disease, and respond to injury quickly. Astrocytes produce neuroprotective factors in the injured brain to clear cellular debris and to orchestrate neurorestorative processes that are beneficial for neurological recovery after traumatic brain injury (TBI). However, astrocytes also become dysregulated and produce cytotoxic mediators that hinder CNS repair by induction of neuronal dysfunction and cell death. Hence, we discuss the potential role of astrocytes in neuropathological processes such as neuroinflammation, neurogenesis, synaptogenesis and blood-brain barrier repair after TBI. Thus, an improved understanding of the dual role of astrocytes may advance our knowledge of post-brain injury recovery, and provide opportunities for the development of novel therapeutic strategies for TBI.

摘要

星形胶质细胞在健康和疾病状态下控制着神经系统的许多过程,并能迅速对损伤做出反应。星形胶质细胞在受损大脑中产生神经保护因子,以清除细胞碎片,并协调神经修复过程,这对创伤性脑损伤 (TBI) 后的神经功能恢复是有益的。然而,星形胶质细胞也会失调,并产生细胞毒性介质,通过诱导神经元功能障碍和细胞死亡来阻碍中枢神经系统修复。因此,我们讨论了星形胶质细胞在神经病理学过程中的潜在作用,如创伤性脑损伤后的神经炎症、神经发生、突触发生和血脑屏障修复。因此,对星形胶质细胞的双重作用有了更好的理解,可能会促进我们对脑损伤后恢复的认识,并为创伤性脑损伤的新治疗策略的发展提供机会。

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[1]
Astrocytes in the Traumatic Brain Injury: the Good and the Bad.

Exp Neurol. 2022-2

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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引用本文的文献

[1]
The Flavonoid Agathisflavone Attenuates Glia Activation After Mechanical Injury of Cortical Tissue and Negatively Regulates Both NRLP3 and IL-1β Expression.

Int J Mol Sci. 2025-2-1

[2]
High-altitude hypoxia aggravated neurological deficits in mice induced by traumatic brain injury via BACH1 mediating astrocytic ferroptosis.

Cell Death Discov. 2025-2-5

[3]
Astrocyte-neuron crosstalk through extracellular vesicle-shuttled miRNA-382-5p promotes traumatic brain injury.

Exp Mol Med. 2024-12

[4]
Candidate Molecular Biomarkers of Traumatic Brain Injury: A Systematic Review.

Biomolecules. 2024-10-11

[5]
Enhancing neurogenesis after traumatic brain injury: The role of adenosine kinase inhibition in promoting neuronal survival and differentiation.

Exp Neurol. 2024-11

[6]
Neurodegenerative Diseases: Unraveling the Heterogeneity of Astrocytes.

Cells. 2024-5-27

[7]
Impacts of PI3K/protein kinase B pathway activation in reactive astrocytes: from detrimental effects to protective functions.

Neural Regen Res. 2025-4-1

[8]
Neuroinflammation and neurodegeneration following traumatic brain injuries.

Anat Sci Int. 2025-1

[9]
Glial cells react to closed head injury in a distinct and spatiotemporally orchestrated manner.

Sci Rep. 2024-1-30

[10]
Enhancing axonal myelination: Clemastine attenuates cognitive impairment in a rat model of diffuse traumatic brain injury.

Transl Res. 2024-6

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