Inflammation in pathogenesis of chronic pain: Foe and friend.
Inflammation in pathogenesis of chronic pain: Foe and friend.
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DOI：
10.1177/17448069231178176
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发表时间：
2023-01
期刊：
影响因子：
3.3
通讯作者：
中科院分区：
文献类型：
--
作者：
慢性疼痛是世界范围内的难治性健康疾病，给个人和社会造成巨大的经济负担。越来越多的证据表明，周围神经系统（PNS）和中枢神经系统（CNS）的炎症是慢性疼痛发病机制的主要因素。早期和晚期的炎症可能对疼痛的开始和消退有不同的影响，这可以被视为朋友或敌人。一方面，疼痛性损伤导致PNS中神经胶质细胞和免疫细胞的活化，释放促炎介质，其有助于伤害感受器的敏化，导致慢性疼痛; CNS中的神经炎症驱动中枢敏化并促进慢性疼痛的发展。另一方面，PNS和CNS的巨噬细胞和神经胶质细胞通过抗炎介质和专门的促缓解介质（SPM）促进疼痛缓解。在这篇综述中，我们提供了一个概述目前的理解炎症的恶化和解决疼痛。此外，我们总结了一些新的策略，可用于通过控制炎症来预防和治疗慢性疼痛。全面认识炎症与慢性疼痛的关系及其具体机制，将为慢性疼痛的治疗提供新的靶点。
Chronic pain is a refractory health disease worldwide causing an enormous economic burden on individuals and society. Accumulating evidence suggests that inflammation in the peripheral nervous system (PNS) and central nervous system (CNS) is the major factor in the pathogenesis of chronic pain. The inflammation in the early- and late phase may have distinctive effects on the initiation and resolution of pain, which can be viewed as friend or foe. On the one hand, painful injuries lead to the activation of glial cells and immune cells in the PNS, releasing pro-inflammatory mediators, which contribute to the sensitization of nociceptors, leading to chronic pain; neuroinflammation in the CNS drives central sensitization and promotes the development of chronic pain. On the other hand, macrophages and glial cells of PNS and CNS promote pain resolution via anti-inflammatory mediators and specialized pro-resolving mediators (SPMs). In this review, we provide an overview of the current understanding of inflammation in the deterioration and resolution of pain. Further, we summarize a number of novel strategies that can be used to prevent and treat chronic pain by controlling inflammation. This comprehensive view of the relationship between inflammation and chronic pain and its specific mechanism will provide novel targets for the treatment of chronic pain.
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DOI：
10.1074/jbc.r117.783076
发表时间：
2017-07-28
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Asatryan A;Bazan NG
通讯作者：
Bazan NG
影响因子：
16.2
作者：
Clements MP;Byrne E;Camarillo Guerrero LF;Cattin AL;Zakka L;Ashraf A;Burden JJ;Khadayate S;Lloyd AC;Marguerat S;Parrinello S
通讯作者：
Parrinello S
影响因子：
15.9
作者：
Arnardottir, Hildur;Thul, Silke;Back, Magnus
通讯作者：
Back, Magnus
影响因子：
64.5
作者：
Basbaum AI;Bautista DM;Scherrer G;Julius D
通讯作者：
Julius D
影响因子：
6.5
作者：
Butovich, IA
通讯作者：
Butovich, IA