Chen Shijie, Zhang Haijun, Wang Zhaoheng, Zhu Daxue, Li Yanhu, Zhang Yizhi, Wang Dongxin, Chen Shuwei, Liu Huan, Kang Xuewen
Lanzhou University Second Hospital, Lanzhou, People's Republic of China.
Orthopaedics Key Laboratory of Gansu Province, Lanzhou, People's Republic of China.
Cell Prolif. 2025 Jun 9:e70068. doi: 10.1111/cpr.70068.
In recent years, a growing number of studies have disclosed the substantial role of macrophages-key immune cells-in the pathological process of intervertebral disc degeneration. Researchers have categorised macrophage phenotypes into M1 and M2 polarisation, associating these polarisations with intervertebral disc degeneration. Essentially, macrophage phenotypes can be classified as either pro-inflammatory or anti-inflammatory. Induced by diverse factors, these distinct polarisation states exert contrary effects on disc injury and repair. Although numerous studies focus on the polarisation of macrophages and the cytokines they secrete in relation to intervertebral disc degeneration, these studies frequently neglect the relationship between the efferocytosis of macrophages and the progression of intervertebral disc degeneration. Efferocytosis is a specialised procedure in which phagocytes, such as macrophages, engulf and eliminate apoptotic cells. This process is crucial for maintaining tissue homeostasis and resolving inflammation. By effectively clearing these dying cells, efferocytosis helps prevent the release of potentially detrimental cellular contents, thereby facilitating healing and the resolution of inflammation. Simultaneously, macrophages digest the engulfed cell debris and release various cytokines that participate in tissue self-repair. Therefore, this article presents an overview of the molecular mechanisms connecting macrophages and their efferocytosis activity to intervertebral disc degeneration, explores new directions for the utilisation of macrophages in the treatment of intervertebral disc degeneration, and discusses the future prospects for the development of therapeutic targets.
近年来，越来越多的研究揭示了巨噬细胞（关键免疫细胞）在椎间盘退变病理过程中的重要作用。研究人员已将巨噬细胞表型分为M1和M2极化，并将这些极化与椎间盘退变联系起来。本质上，巨噬细胞表型可分为促炎或抗炎。由多种因素诱导，这些不同的极化状态对椎间盘损伤和修复产生相反的影响。尽管众多研究聚焦于巨噬细胞极化及其分泌的细胞因子与椎间盘退变的关系，但这些研究常常忽视巨噬细胞的噬菌作用与椎间盘退变进展之间的关系。噬菌作用是一种特殊过程，其中吞噬细胞（如巨噬细胞）吞噬并清除凋亡细胞。这一过程对于维持组织稳态和消除炎症至关重要。通过有效清除这些垂死细胞，噬菌作用有助于防止潜在有害细胞内容物的释放，从而促进愈合和炎症消退。同时，巨噬细胞消化吞噬的细胞碎片并释放参与组织自我修复的各种细胞因子。因此，本文概述了将巨噬细胞及其噬菌作用活性与椎间盘退变联系起来的分子机制，探索巨噬细胞在治疗椎间盘退变中的新应用方向，并讨论治疗靶点开发的未来前景。
