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在神经病变性疼痛中,微质衍生的神经炎症路径

Weiyu Pu^1,2,3, Lingji Zhou^1,3, Renyan Liu^1,3

¹Department of Pain Medicine, The Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.

The Korean journal of pain

|December 10, 2025

概括

神经病痛 (NP) 涉及神经损伤,并由微质激活加剧. 本综述详细介绍了新的NP治疗方法的信号通路和治疗目标.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

神经病痛 (NP) 是一种由神经系统损伤引起的衰弱性慢性疼痛状况.
微质在NP启动和进展中发挥着至关重要的作用,但机制尚未完全理解.
目前的NP治疗方法有限,严重影响患者的生活质量.

研究的目的:

审查微质在神经病痛中的作用.
探索参与微质激活的关键信号通路 (NF-κB,PI3K/Akt/mTOR,p38MAPK,JAK2/STAT3,Nrf2/HO-1) 的研究.
总结目前和未来的针对NP的微质向疗法.

主要方法:

关于神经病痛中微质激活的最新研究的文献综述.
分析主要信号通路中的关键分子.
药物,化合物和非侵入性治疗应用的概述.

主要成果:

确定了关键信号通路 (NF-κB,PI3K/Akt/mTOR,p38MAPK,JAK2/STAT3,Nrf2/HO-1) 在NP中调解微质激活.
详细介绍了微质表型,炎症过程和NP之间的相互作用.
突出了潜在的治疗剂和针对微质细胞的非侵入性策略.

结论:

微质是神经病痛病原体的核心.
了解这些信号通路为开发针对小质细胞的新型NP疗法提供了基础.
对这些途径和治疗方法的进一步研究有望改善NP管理.

关键词:

微质细胞中的微质细胞与NF-E2相关的因素2 在 NF-kappa B B 里.神经疼痛是一种神经疼痛.神经炎症性疾病神经炎症性疾病酸氨基醇3 - 酸酶.原始瘤基因蛋白质c-aktakt是什么意思在TOR中,氨酸-氨酸激酶 (Serine-Threonine Kinases) 发生.

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