游戏中的新角色:确定 C1ql1 为驱动 OPC 分化的新因素。

Jana Van Broeckhoven, Femke Mussen, Melissa Schepers, Tim Vanmierlo, Niels Hellings
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引用次数: 0

摘要

少突胶质细胞(OLG)是中枢神经系统(CNS)中产生髓鞘的细胞。受伤后,这些细胞容易死亡,导致脱髓鞘,最终导致轴突丢失和神经变性。损伤后,受损的中枢神经系统会在病变部位重新填充少突胶质前体细胞(OPCs),这些细胞随后会成熟为OLGs,以修复髓鞘损伤并防止轴突进一步丧失。在本期文章中,Altunay 等人发现,补体成分 1 q 亚组分样-1(C1ql1)--一种已知在神经元-神经元突触中发挥作用的因子--也在 OPCs 中表达,并促使它们分化为 OLGs。这些数据表明,C1ql1或其他下游因子可能成为脱髓鞘疾病(如多发性硬化症(MS))的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A new player in the game: identification of C1ql1 as a novel factor driving OPC differentiation.

Oligodendrocytes (OLGs) are the myelin-producing cells in the central nervous system (CNS). Following injury, these cells are prone to death, leading to demyelination and, eventually, axonal loss and neurodegeneration. Upon injury, the damaged CNS repopulates the lesion with oligodendrocyte precursor cells (OPCs) that consequently mature into OLGs to repair the myelin damage and prevent further axonal loss. In this issue, Altunay et al. identified that complement component 1, q subcomponent-like-1 (C1ql1), a factor known to play a role in neuron-neuron synapses, is also expressed by OPCs and drives their differentiation into OLGs. These data suggest that C1ql1 or other downstream factors could be therapeutic targets in the context of demyelinating disorders in which remyelination fails, such as in multiple sclerosis (MS).

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