Astrocyte-mediated mechanisms contribute to traumatic brain injury pathology.
Astrocyte-mediated mechanisms contribute to traumatic brain injury pathology.
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DOI：
10.1002/wsbm.1622
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发表时间：
2023-06
影响因子：
3.1
通讯作者：
C. Muñoz-Ballester;S. Robel
中科院分区：
文献类型：
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作者：
C. Muñoz-Ballester;S. Robel
星形胶质细胞通过改变其分子组成和细胞生物学来响应创伤性脑损伤（TBI），从而导致星形胶质细胞功能的变化。这些变化可能是适应性的，启动大脑中的修复过程，也可能是有害的，导致继发性损伤，包括神经元死亡或神经元活动异常。星形胶质细胞对 TBI 的反应常常（但并非总是）伴随着中间丝的上调，包括神经胶质纤维酸性蛋白 (GFAP) 和波形蛋白。由于 GFAP 通常在神经系统紊乱的情况下上调，因此反应性星形胶质细胞增生有时被视为“全有或全无”的过程。然而，对于每种 TBI 类型，甚至对于同一受伤大脑中的每个星形胶质细胞，星形胶质细胞的细胞、分子和生理调节程度并不相同。此外，新的研究强调，不同的神经损伤和疾病会导致完全独特的、有时甚至是不同的星形胶质细胞变化。因此，将星形胶质细胞生物学的发现从一种病理背景推断到另一种病理背景是有问题的。我们总结了目前关于星形胶质细胞对 TBI 的反应的知识，并指出了该领域应该解决的开放性问题，以更好地了解星形胶质细胞如何影响 TBI 的结果。我们讨论星形胶质细胞对局灶性与弥漫性 TBI 的反应以及同一大脑内反应性星形胶质细胞的异质性、中间丝上调的作用、星形胶质细胞功能的功能变化（包括钾和谷氨酸稳态）、血脑屏障维持和修复、代谢和活性氧解毒、性别差异以及 TBI 后影响星形胶质细胞增殖的因素。本文分类为：神经系统疾病 > 分子和细胞生理学。
Astrocytes respond to traumatic brain injury (TBI) with changes to their molecular make-up and cell biology, which results in changes in astrocyte function. These changes can be adaptive, initiating repair processes in the brain, or detrimental, causing secondary damage including neuronal death or abnormal neuronal activity. The response of astrocytes to TBI is often-but not always-accompanied by the upregulation of intermediate filaments, including glial fibrillary acidic protein (GFAP) and vimentin. Because GFAP is often upregulated in the context of nervous system disturbance, reactive astrogliosis is sometimes treated as an "all-or-none" process. However, the extent of astrocytes' cellular, molecular, and physiological adjustments is not equal for each TBI type or even for each astrocyte within the same injured brain. Additionally, new research highlights that different neurological injuries and diseases result in entirely distinctive and sometimes divergent astrocyte changes. Thus, extrapolating findings on astrocyte biology from one pathological context to another is problematic. We summarize the current knowledge about astrocyte responses specific to TBI and point out open questions that the field should tackle to better understand how astrocytes shape TBI outcomes. We address the astrocyte response to focal versus diffuse TBI and heterogeneity of reactive astrocytes within the same brain, the role of intermediate filament upregulation, functional changes to astrocyte function including potassium and glutamate homeostasis, blood-brain barrier maintenance and repair, metabolism, and reactive oxygen species detoxification, sex differences, and factors influencing astrocyte proliferation after TBI. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology.