Research progress on endoplasmic reticulum stress mechanisms in chronic pain
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.