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少突胶质细胞衍生细胞外囊泡对轴突的支持机制。

Mechanisms of axonal support by oligodendrocyte-derived extracellular vesicles.

机构信息

Institute of Developmental Biology and Neurobiology, Johannes Gutenberg University Mainz, Mainz, Germany.

Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.

出版信息

Nat Rev Neurosci. 2023 Aug;24(8):474-486. doi: 10.1038/s41583-023-00711-y. Epub 2023 May 31.

DOI:10.1038/s41583-023-00711-y
PMID:37258632
Abstract

Extracellular vesicles (EVs) have recently emerged as versatile elements of cell communication in the nervous system, mediating tissue homeostasis. EVs influence the physiology of their target cells via horizontal transfer of molecular cargo between cells and by triggering signalling pathways. In this Review, we discuss recent work revealing that EVs mediate interactions between oligodendrocytes and neurons, which are relevant for maintaining the structural integrity of axons. In response to neuronal activity, myelinating oligodendrocytes release EVs, which are internalized by neurons and provide axons with key factors that improve axonal transport, stress resistance and energy homeostasis. Glia-to-neuron transfer of EVs is thus a crucial facet of axonal preservation. When glial support is impaired, axonal integrity is progressively lost, as observed in myelin-related disorders, other neurodegenerative diseases and with normal ageing. We highlight the mechanisms that oligodendroglial EVs use to sustain axonal integrity and function.

摘要

细胞外囊泡 (EVs) 最近作为神经系统中细胞通讯的多功能元件出现,介导组织稳态。EVs 通过细胞间分子货物的水平转移和触发信号通路来影响靶细胞的生理学。在这篇综述中,我们讨论了最近的工作,揭示了 EVs 介导少突胶质细胞和神经元之间的相互作用,这对于维持轴突的结构完整性很重要。髓鞘形成的少突胶质细胞在神经元活动时释放 EVs,神经元将其内化,并为轴突提供关键因子,改善轴突运输、应激抗性和能量稳态。因此,EV 从胶质细胞到神经元的转移是轴突保存的关键方面。当神经胶质支持受损时,轴突完整性逐渐丧失,如在与髓鞘相关的疾病、其他神经退行性疾病和正常衰老中观察到的那样。我们强调了少突胶质细胞 EVs 用于维持轴突完整性和功能的机制。

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