Nasir Abdul, Afridi Maryam, Afridi Ome Kalsoom, Khan Muhammad Arif, Khan Amir, Zhang Jun, Qian Bai
Department of Anesthesiology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, China; Medical Research Center, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, China.
Department of Pharmacy, Qurtuba University, Peshawar, KP, Pakistan.
Neurosci Biobehav Rev. 2025 Jun;173:106162. doi: 10.1016/j.neubiorev.2025.106162. Epub 2025 Apr 14.
The transition from acute to chronic pain is a complex and multifactorial process that presents significant challenges in both diagnosis and treatment. Key mechanisms of peripheral and central sensitization, neuroinflammation, and altered synaptic plasticity contribute to the amplification of pain signals and the persistence of pain. Glial cell activation, particularly microglia and astrocytes, is pivotal in developing chronic pain by releasing pro-inflammatory cytokines that enhance pain sensitivity. This review explores the molecular, cellular, and systemic mechanisms underlying the transition from acute to chronic pain, offering new insights into the molecular and neurobiological mechanisms involved, which are often underexplored in existing literature. It also addresses emerging therapeutic strategies beyond traditional pain management, offering valuable perspectives for future research and clinical applications.
从急性疼痛向慢性疼痛的转变是一个复杂的多因素过程，在诊断和治疗方面都带来了重大挑战。外周和中枢敏化、神经炎症以及突触可塑性改变等关键机制，促成了疼痛信号的放大和疼痛的持续存在。胶质细胞激活，尤其是小胶质细胞和星形胶质细胞，通过释放增强疼痛敏感性的促炎细胞因子，在慢性疼痛的形成中起关键作用。本综述探讨了从急性疼痛向慢性疼痛转变背后的分子、细胞和全身机制，为相关分子和神经生物学机制提供了新的见解，而这些机制在现有文献中往往未得到充分研究。它还讨论了传统疼痛管理之外的新兴治疗策略，为未来研究和临床应用提供了有价值的观点。
