Li Hongtao, Pan Hongyu, Xiao Changming, Li Hanyue, Long Longhai, Wang Xiaoqiang, Luo Shengyu, Lyu Kexin, Chen Yixuan, Jiang Li, Lu Jingwei, Shen Huarui, Li Sen
Department of Spinal Surgery, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Sichuan, China.
School of Physical Education, Southwest Medical University, Luzhou, China.
Heliyon. 2023 Sep 7;9(9):e19951. doi: 10.1016/j.heliyon.2023.e19951. eCollection 2023 Sep.
Intervertebral disc degeneration (IDD) has been widely recognized as the primary cause of low back pain and is one of the major chronic diseases imposing a severe socioeconomic burden worldwide. IDD is a degenerative process characterized by inflammatory responses, and its underlying pathological mechanisms remain complex. Genetic, developmental, biochemical, and biomechanical factors contribute to the development of IDD. There is a pressing need for an effective non-surgical treatment, mainly due to the lack of comprehensive understanding of the specific mechanisms involved and the effective therapeutic targets for IDD. Recently, interleukin (IL)-1β has been recognized as an essential inflammatory factor and a key mediator of the inflammatory process in IDD. Current studies have found that IL-1β is mainly involved in IDD by affecting the metabolism of the extracellular matrix and regulating cell death (RCD), such as apoptosis, pyroptosis, and ferroptosis (a new form of RCD). Although analysis of clinical samples from different laboratories confirmed how IL-1β is induced in IDD, its specific signal transduction pathway, and the inflammatory role mediated in IDD remains unclear. This review describes the molecules and mechanisms involved in IL-1β-mediated inflammatory responses, and their roles in resolving the inflammatory process in IDD. Understanding the signaling pathways involved in IL-1β may lead to a new class of targets that promote remission for IDD patients. This review aims to provide a framework for the treatment of IDD by analyzing the signaling mechanism and function related to IL-1β, especially in terms of inflammation, matrix metabolism, and cell death regulation.
椎间盘退变（IDD）已被广泛认为是腰痛的主要原因，也是给全球带来严重社会经济负担的主要慢性疾病之一。IDD是一个以炎症反应为特征的退行性过程，其潜在的病理机制仍然复杂。遗传、发育、生化和生物力学因素都促成了IDD的发展。由于对IDD所涉及的具体机制和有效治疗靶点缺乏全面了解，迫切需要一种有效的非手术治疗方法。最近，白细胞介素（IL）-1β已被认为是IDD炎症过程中的一种重要炎症因子和关键介质。目前的研究发现，IL-1β主要通过影响细胞外基质的代谢和调节细胞死亡（RCD），如凋亡、焦亡和铁死亡（一种新的RCD形式）来参与IDD。尽管来自不同实验室的临床样本分析证实了IL-1β在IDD中是如何被诱导的，但其具体的信号转导途径以及在IDD中介导的炎症作用仍不清楚。本综述描述了IL-1β介导的炎症反应所涉及的分子和机制，以及它们在解决IDD炎症过程中的作用。了解IL-1β所涉及的信号通路可能会产生一类新的靶点，从而促进IDD患者的病情缓解。本综述旨在通过分析与IL-1β相关的信号机制和功能，特别是在炎症、基质代谢和细胞死亡调节方面，为IDD的治疗提供一个框架。
