Inhibitory milieu at the multiple sclerosis lesion site and the challenges for remyelination.,Glia

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Inhibitory milieu at the multiple sclerosis lesion site and the challenges for remyelination.
Glia ( IF 5.4 ) Pub Date : 2019-08-23 , DOI: 10.1002/glia.23711
Dylan A Galloway ₁ , Elizabeth Gowing ₂ , Solmaz Setayeshgar ₃ , Rashmi Kothary _{4,

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Affiliation

Regeneration of myelin, following injury, can occur within the central nervous system to reinstate proper axonal conductance and provide trophic support. Failure to do so renders the axons vulnerable, leading to eventual degeneration, and neuronal loss. Thus, it is essential to understand the mechanisms by which remyelination or failure to remyelinate occur, particularly in the context of demyelinating and neurodegenerative disorders. In multiple sclerosis, oligodendrocyte progenitor cells (OPCs) migrate to lesion sites to repair myelin. However, during disease progression, the ability of OPCs to participate in remyelination diminishes coincident with worsening of the symptoms. Remyelination is affected by a broad range of cues from intrinsic programming of OPCs and extrinsic local factors to the immune system and other systemic elements including diet and exercise. Here we review the literature on these diverse inhibitory factors and the challenges they pose to remyelination. Results spanning several disciplines from fundamental preclinical studies to knowledge gained in the clinic will be discussed.

中文翻译：

多发性硬化病变部位的抑制性环境和髓鞘再生的挑战。

损伤后，髓磷脂的再生可在中枢神经系统内发生，以恢复适当的轴突传导并提供营养支持。否则，轴突变得脆弱，最终导致变性和神经元丢失。因此，必须了解发生髓鞘再生或髓鞘再生失败的机制，特别是在脱髓鞘和神经退行性疾病的情况下。在多发性硬化症中，少突胶质细胞祖细胞（OPC）迁移到病变部位以修复髓磷脂。但是，在疾病发展过程中，OPC参与髓鞘再生的能力会随着症状的恶化而降低。髓鞘再生受到多种提示的影响，从OPC的内在编程和外在的局部因素到免疫系统和其他系统性元素，包括饮食和运动。在这里，我们回顾了有关这些不同抑制因子及其对髓鞘再生构成的挑战的文献。将讨论从基础临床前研究到临床知识等多个学科的研究结果。

更新日期：2019-08-23

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