Glia as a Link between Neuroinflammation and Neuropathic Pain.
Glia as a Link between Neuroinflammation and Neuropathic Pain.
复制标题
DOI：
10.4110/in.2012.12.2.41
复制
发表时间：
2012-04
期刊：
影响因子：
6
通讯作者：
Suk K
中科院分区：
文献类型：
--
作者：
Jha MK;Jeon S;Suk K
当代研究表明，外周损伤激活了外周和中枢细胞回路的神经胶质成分。神经胶质应激源或激活信号的随后释放有助于神经病理性疼痛和神经炎症。最近的研究记录了神经胶质在神经性疼痛和神经炎症的发展和持续中作为连接环节的重要性，从而将注意力集中在神经胶质病理学上，作为基本上所有年龄相关的神经退行性疾病的一般潜在因素。人们普遍认为，过度的胶质细胞活化是神经系统疾病的一个关键过程，涉及强促炎细胞因子的释放，这可能引发多种疾病状态的恶化。本文将简要讨论最近的研究结果，阐明了神经胶质细胞作为神经病理性疼痛和神经炎症之间的联系的分子和细胞机制。
Contemporary studies illustrate that peripheral injuries activate glial components of the peripheral and central cellular circuitry. The subsequent release of glial stressors or activating signals contributes to neuropathic pain and neuroinflammation. Recent studies document the importance of glia in the development and persistence of neuropathic pain and neuroinflammation as a connecting link, thereby focusing attention on the glial pathology as the general underlying factor in essentially all age-related neurodegenerative diseases. There is wide agreement that excessive glial activation is a key process in nervous system disorders involving the release of strong pro-inflammatory cytokines, which can trigger worsening of multiple disease states. This review will briefly discuss the recent findings that have shed light on the molecular and cellular mechanisms of glia as a connecting link between neuropathic pain and neuroinflammation.