Hyperalgesic Priming in the Transition From Acute to Chronic Pain: Focus on Different Models and the Molecular Mechanisms Involved.

Abstract

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.