白细胞介素-17A介导炎症反应与椎间盘退变

Interleukin-17A mediated inflammatory responses in intervertebral disc degeneration

椎间盘退变(intervertebral disc degeneration,IDD)是引起腰背痛的主要原因之一。IDD的发病机制复杂,与年龄、创伤、遗传易感性、自身免疫炎症反应等有关。研究表明,白细胞介素在IDD中扮演着重要的角色,白细胞介素通过介导椎间盘内炎症反应,促进细胞外基质降解以及椎间盘细胞凋亡来加速IDD的病理过程。白细胞介素-17(interleukin-17,IL-17A)在退变的椎间盘中高表达,提示其作为一种重要的炎症因子,参与IDD病理生理过程。IL-17A通过诱导炎症细胞因子、细胞外基质降解相关因子以及趋化因子等的产生,促进IDD的发生与发展。本文旨在探讨IL-17A在椎间盘中的产生与作用以及其介导IDD发生、发展的分子机制,为防治IDD提供新思路。

Intervertebral disc degeneration(IDD)is one of the primary causes of low back pain.The pathogenesis of IDD is intricate and involves factors such as age,trauma,genetic susceptibility,and autoimmune inflammatory responses.Research indicates that interleukin-17(IL-17A)plays a crucial role in IDD by mediating intra-discal inflammation,promoting extracellular matrix degradation,and accelerating intervertebral disc cell apoptosis,thereby expediting the pathological process of IDD.IL-17A is highly expressed in degenerated intervertebral discs,suggesting its importance as an inflammatory factor in the pathophysiological processes of IDD.IL-17A induces the production of inflammatory cytokines,factors related to extracellular matrix degradation,and chemokines,thus promoting the occurrence and development of IDD.This article aims to explore the production and function of IL-17A within intervertebral discs and its role in mediating the occurrence and progression of IDD,offering new insights for the prevention and treatment of IDD.