Suppr超能文献

脱髓鞘疾病小鼠模型中神经炎症的分子触发因素。

Molecular triggers of neuroinflammation in mouse models of demyelinating diseases.

出版信息

Biol Chem. 2013 Dec;394(12):1571-81. doi: 10.1515/hsz-2013-0219.

Abstract

Myelinating cells wrap axons with multi-layered myelin sheaths for rapid impulse propagation. Dysfunctions of oligodendrocytes or Schwann cells are often associated with neuroinflammation, as observed in animal models of leukodystrophies and peripheral neuropathies, respectively. The neuroinflammatory response modulates the pathological changes, including demyelination and axonal injury, but also remyelination and repair. Here we discuss different immune mechanisms as well as factors released or exposed by myelinating glia in disease conditions. The spectrum of inflammatory mediators varies with different myelin disorders and has a major impact on the beneficial or detrimental role of immune cells in keeping nervous system integrity.

摘要

少突胶质细胞或施万细胞的功能障碍通常与神经炎症有关,分别在脑白质营养不良和周围神经病变的动物模型中观察到。神经炎症反应调节病理变化,包括脱髓鞘和轴突损伤,但也调节髓鞘再生和修复。在这里,我们讨论了不同的免疫机制,以及髓鞘形成胶质细胞在疾病状态下释放或暴露的因子。炎症介质的谱随不同的髓鞘疾病而变化,对免疫细胞在保持神经系统完整性方面的有益或有害作用有重大影响。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验