Emerging targets in neuroinflammation-driven chronic pain.

Emerging targets in neuroinflammation-driven chronic pain.
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神经炎症驱动的慢性疼痛的新兴目标。

DOI:
10.1038/nrd4334
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发表时间:
2014-07
影响因子:
120.1
通讯作者:
Gao, Yong-Jing
Gao, Yong-Jing
中科院分区:
医学1区
文献类型:
--
作者:
Ji, Ru-Rong;Xu, Zhen-Zhong;Gao, Yong-Jing

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目前的镇痛药主要调节神经元中的疼痛转导和传递,并且在控制疾病进展方面的成功有限。越来越多的证据表明,以免疫细胞浸润、胶质细胞活化和外周和中枢神经系统炎症介质产生为特征的神经炎症在慢性疼痛的诱导和维持中具有重要作用。本文综述了促进脊髓神经炎症和慢性疼痛的新兴靶点,如趋化因子,蛋白酶和Wnt通路。它还强调了抗炎和促消退脂质介质作用于免疫细胞,神经胶质细胞和神经元,以解决神经炎症,突触可塑性和疼痛。针对过度的神经炎症可以为慢性疼痛和相关的神经和精神疾病提供新的治疗机会。
Current analgesics predominately modulate pain transduction and transmission in neurons and have limited success in controlling disease progression. Accumulating evidence suggests that neuroinflammation, which is characterized by infiltration of immune cells, activation of glial cells and production of inflammatory mediators in the peripheral and central nervous system, has an important role in the induction and maintenance of chronic pain. This review focuses on emerging targets such as chemokines, proteases and the Wnt pathway that promote spinal cord neuroinflammation and chronic pain. It also highlights the anti-inflammatory and pro-resolution lipid mediators that act on immune cells, glial cells and neurons to resolve neuroinflammation, synaptic plasticity and pain. Targeting excessive neuroinflammation could offer new therapeutic opportunities for chronic pain and related neurological and psychiatric disorders.
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