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创伤性脑损伤中的反应性胶质增生:综述

Reactive gliosis in traumatic brain injury: a comprehensive review.

作者信息

Amlerova Zuzana, Chmelova Martina, Anderova Miroslava, Vargova Lydia

机构信息

Department of Neuroscience, Second Faculty of Medicine, Charles University, Prague, Czechia.

Department of Cellular Neurophysiology, Institute of Experimental Medicine of the Czech Academy of Sciences, Prague, Czechia.

出版信息

Front Cell Neurosci. 2024 Feb 28;18:1335849. doi: 10.3389/fncel.2024.1335849. eCollection 2024.

Abstract

Traumatic brain injury (TBI) is one of the most common pathological conditions impacting the central nervous system (CNS). A neurological deficit associated with TBI results from a complex of pathogenetic mechanisms including glutamate excitotoxicity, inflammation, demyelination, programmed cell death, or the development of edema. The critical components contributing to CNS response, damage control, and regeneration after TBI are glial cells-in reaction to tissue damage, their activation, hypertrophy, and proliferation occur, followed by the formation of a glial scar. The glial scar creates a barrier in damaged tissue and helps protect the CNS in the acute phase post-injury. However, this process prevents complete tissue recovery in the late/chronic phase by producing permanent scarring, which significantly impacts brain function. Various glial cell types participate in the scar formation, but this process is mostly attributed to reactive astrocytes and microglia, which play important roles in several brain pathologies. Novel technologies including whole-genome transcriptomic and epigenomic analyses, and unbiased proteomics, show that both astrocytes and microglia represent groups of heterogenic cell subpopulations with different genomic and functional characteristics, that are responsible for their role in neurodegeneration, neuroprotection and regeneration. Depending on the representation of distinct glia subpopulations, the tissue damage as well as the regenerative processes or delayed neurodegeneration after TBI may thus differ in nearby or remote areas or in different brain structures. This review summarizes TBI as a complex process, where the resultant effect is severity-, region- and time-dependent and determined by the model of the CNS injury and the distance of the explored area from the lesion site. Here, we also discuss findings concerning intercellular signaling, long-term impacts of TBI and the possibilities of novel therapeutical approaches. We believe that a comprehensive study with an emphasis on glial cells, involved in tissue post-injury processes, may be helpful for further research of TBI and be the decisive factor when choosing a TBI model.

摘要

创伤性脑损伤(TBI)是影响中枢神经系统(CNS)的最常见病理状况之一。与TBI相关的神经功能缺损源于一系列复杂的发病机制,包括谷氨酸兴奋性毒性、炎症、脱髓鞘、程序性细胞死亡或水肿的形成。对TBI后CNS反应、损伤控制和再生起关键作用的成分是胶质细胞——对组织损伤作出反应时,它们会激活、肥大并增殖,随后形成胶质瘢痕。胶质瘢痕在受损组织中形成一道屏障,有助于在损伤后的急性期保护CNS。然而,这一过程会通过产生永久性瘢痕而阻碍组织在晚期/慢性期的完全恢复,从而对脑功能产生重大影响。多种胶质细胞类型参与瘢痕形成,但这一过程主要归因于反应性星形胶质细胞和小胶质细胞,它们在多种脑部病变中发挥重要作用。包括全基因组转录组学和表观基因组学分析以及非靶向蛋白质组学在内的新技术表明,星形胶质细胞和小胶质细胞均代表具有不同基因组和功能特征的异质性细胞亚群,这些特征决定了它们在神经退行性变、神经保护和再生中的作用。根据不同胶质细胞亚群的表现,TBI后的组织损伤以及再生过程或延迟性神经退行性变在附近或远处区域或不同脑结构中可能会有所不同。本综述将TBI总结为一个复杂的过程,其最终影响取决于严重程度、区域和时间,并由CNS损伤模型以及探索区域与损伤部位的距离决定。在此,我们还讨论了关于细胞间信号传导、TBI的长期影响以及新型治疗方法可能性的研究结果。我们认为,着重研究参与损伤后组织过程的胶质细胞的综合性研究,可能有助于TBI的进一步研究,并在选择TBI模型时起决定性作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b57e/10933082/8f1c06a78096/fncel-18-1335849-g001.jpg

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