摘要
中枢神经系统(CNS)针对一系列有关键意义的胶质细胞增生反应显示了动态免疫和炎症反应,中枢神经系统中的神经胶质细胞不仅作为来源,而且是目标促炎介质。毫无疑问,这些细胞有效地处理了组织碎片以及促进了创面的愈合及组织修复。然而,这些非神经胶质细胞合成和释放了大量的炎症调节因子,它们可能是有害的神经元,轴突,髓鞘以及神经胶质细胞本身。急性的入侵通常是短暂的,并且不太可能会损害神经元的存活,然而慢性炎症是一个长期和 经常自我维持的反应,在最初受伤或者侵入以后很长时间依然存在。对于不同的神经系统疾病包括阿尔茨海默氏病,它可以作为一个起始点。越来越多的证据表明了代谢紊乱的作用和线粒体破坏神经炎症和神经退行性疾病的发病机制。退行性疾病的特点是增加氧化和内质网应激和自噬缺陷。此外,神经炎症伴有胶质能量代谢的改变。 在这里,我们全面阐述了神经胶质细胞介导的炎症代谢特点以及胶质细胞代谢协调了神经炎症反应和不同神经失控的病理生理学。
关键词: 星形胶质细胞;中枢神经系统;神经元;炎症;神经炎症;神经退行性疾病;代谢;线粒体;小胶质细胞;氧化应激。
Current Alzheimer Research
Title:Metabolic Control of Glia-Mediated Neuroinflammation
Volume: 13 Issue: 4
Author(s): Mithilesh Kumar Jha, Dong Ho Park, Hyun Kook, In-Kyu Lee, Won-Ha Lee, Kyoungho Suk
Affiliation:
关键词: 星形胶质细胞;中枢神经系统;神经元;炎症;神经炎症;神经退行性疾病;代谢;线粒体;小胶质细胞;氧化应激。
摘要: The central nervous system (CNS) shows dynamic immune and inflammatory responses to a variety of insults having crucial implications for reactive gliosis. Glial cells in the CNS serve not only as the source, but also as targets of proinflammatory mediators. Undoubtedly, these cells efficiently work towards the disposal of tissue debris and promotion of wound healing as well as tissue repair. However, these non-neuronal glial cells synthesize and release numerous inflammatory mediators, which can be detrimental to neurons, axons, myelin, and the glia themselves. While an acute insult is typically transient and unlikely to be detrimental to neuronal survival, chronic neuroinflammation is a long-standing and often self-perpetuating response, which persists even long after the initial injury or insult. It can serve as a point of origin for diverse neurological disorders including Alzheimer's disease. Accumulating evidence demonstrates the contribution of metabolic dysfunction and mitochondrial failure to the pathogenesis of neuroinflammatory and neurodegenerative diseases. Neurodegenerative conditions are also characterized by increased oxidative and endoplasmic reticulum stresses and autophagy defects. Furthermore, neuroinflammatory conditions are accompanied by an alteration in glial energy metabolism. Here, we comprehensively review the metabolic hallmarks of glia-mediated neuroinflammation and how the glial metabolic shift orchestrates the neuroinflammatory response and pathophysiology of diverse neurological disorders.
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Cite this article as:
Mithilesh Kumar Jha, Dong Ho Park, Hyun Kook, In-Kyu Lee, Won-Ha Lee, Kyoungho Suk , Metabolic Control of Glia-Mediated Neuroinflammation, Current Alzheimer Research 2016; 13 (4) . https://dx.doi.org/10.2174/1567205013666151116124755
DOI https://dx.doi.org/10.2174/1567205013666151116124755 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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