慢性疼痛中内质网应激机制的研究进展  

Research progress on endoplasmic reticulum stress mechanisms in chronic pain

作　　者：张彩霞[1] 于尚辰 张咸伟[2] ZHANG Cai-xia;YU Shang-chen;ZHANG Xian-wei(Department of Anesthesiology,Wuhan No.1 Hospital,Wuhan 430022,China;Department of Anesthesiology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)

机构地区：[1]武汉市第一医院麻醉科,武汉430022 [2]华中科技大学同济医学院附属同济医院麻醉科,武汉430030

出　　处：《中国疼痛医学杂志》2024年第9期686-690,共5页Chinese Journal of Pain Medicine

摘　　要：慢性疼痛作为公共卫生难题,其发病机制复杂,涉及脊髓神经元兴奋、胶质细胞激活及受体活化等。药物治疗虽能缓解疼痛,但不良反应限制了其应用。研究表明,内质网应激在慢性疼痛中扮演关键角色,通过影响疼痛感受器敏感性、调控伤害信号传递、触发炎症反应及神经可塑性改变,加剧疼痛并促进其发展。本文综述了内质网蛋白激酶样内切割酶(PKR-like endoplasmic reticulum kinase,PERK)、内质网应激调节因子1α (inositol-requiring enzyme 1α, IRE1α)和激活转录因子6 (activating transcription factor 6, ATF6)等通路在内质网应激与慢性疼痛中的具体机制,旨在为其深入研究和临床应用提供科学支撑,并探讨尚未解决的问题及未来发展方向。Chronic pain,as a major public health issue,involves complex pathogenesis,including spinal neuron excitation,glial cell activation,and receptor activation.Although current treatment methods can alleviate pain,their application is limited by adverse effects.Research indicates that endoplasmic reticulum(ER)stress plays a crucial role in chronic pain.By affecting the sensitivity of pain receptors,regulating nociceptive signal transmission,triggering inflammatory responses,and altering neural plasticity,ER stress exacerbates pain and promotes its progression.This review summarizes the specific mechanisms of the pathways involving PKR-like endoplasmic reticulum kinase(PERK),inositol-requiring enzyme 1α(IRE1α),and activating transcription factor 6(ATF6)in ER stress and chronic pain.The aim is to provide scientific support for further research and clinical applications,and to discuss unresolved issues and future research directions.

关 键 词：慢性疼痛 内质网应激 内质网蛋白激酶样内切割酶 内质网应激调节因子1α 激活转录因子6 未折叠蛋白反应 

分 类 号：R402[医药卫生—临床医学]