Zhang Mi, Li Ningbo, Zhao Shuai, Feng Xiaobo
Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Wuhan, 430071, People's Republic of China.
Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
J Pain Res. 2025 Mar 21;18:1491-1501. doi: 10.2147/JPR.S514851. eCollection 2025.
Poorly treated acute pain can develop into chronic pain, resulting in significant impairment of patients' quality of life. The hyperalgesic priming model is commonly used to study how acute pain transforms into chronic pain. Inflammatory factors, small molecules, opioid receptor agonists, chemotherapy drugs, and stress serve as initiating factors in the hyperalgesic priming model. Various signaling pathways such as PKCε, MOR and ephrin-B2 pathways, and sexual differences also contribute to the transformation process of chronic pain. In this review, we examine various hyperalgesic priming models and their underlying molecular mechanisms. By thoroughly investigating these molecular mechanisms, researchers can more precisely identify the critical nodes involved in pain transformation, thereby developing more targeted treatment strategies.
急性疼痛若治疗不当，可能会发展为慢性疼痛，从而严重损害患者的生活质量。痛觉过敏启动模型常用于研究急性疼痛如何转变为慢性疼痛。炎症因子、小分子、阿片受体激动剂、化疗药物和应激是痛觉过敏启动模型中的起始因素。PKCε、MOR和ephrin - B2等多种信号通路以及性别差异也在慢性疼痛的转变过程中发挥作用。在本综述中，我们研究了各种痛觉过敏启动模型及其潜在的分子机制。通过深入研究这些分子机制，研究人员可以更精确地识别疼痛转变过程中的关键节点，从而制定更具针对性的治疗策略。
