Zheng Kaiyuan, Wang Siyu, Deng Meng, Luo Yaomin, Li Wen, Zeng Lianlin, Wang Yinxu
Department of Rehabilitation Medicine, Intensive Care Medicine Affiliated Hospital of North Sichuan Medical College Nanchong China.
Department of Clinical Laboratory The First People's Hospital of Guangyuan Guangyuan China.
JOR Spine. 2025 May 14;8(2):e70065. doi: 10.1002/jsp2.70065. eCollection 2025 Jun.
Intervertebral disc degeneration (IVDD) is a leading cause of low back pain (LBP), contributing significantly to global disability and productivity loss. Its pathogenesis involves complex processes, including inflammation, cellular senescence, angiogenesis, fibrosis, neural ingrowth, and sensitization. Emerging evidence highlights macrophages as central immune regulators infiltrating degenerated discs, with macrophage polarization implicated in IVDD progression. However, the mechanisms linking macrophage polarization to IVDD pathology remain poorly elucidated.
A comprehensive literature review was conducted by searching major databases (PubMed, Web of Science, and Scopus) for studies published in the last decade (2014-2024). Keywords included "intervertebral disc degeneration," "macrophage polarization," "inflammation," "senescence," and "therapeutic strategies." Relevant articles were selected, analyzed, and synthesized to evaluate the role of macrophage polarization in IVDD.
Macrophage polarization dynamically influences IVDD through multiple pathways. Pro-inflammatory M1 macrophages exacerbate disc degeneration by amplifying inflammatory cytokines (e.g., TNF-α, IL-1β), promoting cellular senescence, and stimulating abnormal angiogenesis and neural ingrowth. In contrast, anti-inflammatory M2 macrophages may mitigate degeneration by suppressing inflammation and enhancing tissue repair. Therapeutic strategies targeting macrophage polarization include pharmacological agents (e.g., cytokines, small-molecule inhibitors), biologic therapies, gene editing, and physical interventions. Challenges persist, such as incomplete understanding of polarization triggers, lack of targeted delivery systems, and limited translational success in preclinical models.
Macrophage polarization is a pivotal regulator of IVDD pathology, offering promising therapeutic targets. Future research should focus on elucidating polarization mechanisms, optimizing spatiotemporal control of macrophage phenotypes, and developing personalized therapies. Addressing these challenges may advance innovative strategies to halt or reverse IVDD progression, ultimately improving clinical outcomes for LBP patients.
椎间盘退变(IVDD)是下腰痛(LBP)的主要原因,对全球残疾和生产力损失有重大影响。其发病机制涉及复杂过程,包括炎症、细胞衰老、血管生成、纤维化、神经长入和敏化。新出现的证据表明巨噬细胞是浸润退变椎间盘的核心免疫调节因子,巨噬细胞极化与IVDD进展有关。然而,将巨噬细胞极化与IVDD病理联系起来的机制仍不清楚。
通过检索主要数据库(PubMed、Web of Science和Scopus),对过去十年(2014 - 2024年)发表的研究进行全面文献综述。关键词包括“椎间盘退变”、“巨噬细胞极化”、“炎症”、“衰老”和“治疗策略”。选择、分析和综合相关文章,以评估巨噬细胞极化在IVDD中的作用。
巨噬细胞极化通过多种途径动态影响IVDD。促炎M1巨噬细胞通过放大炎性细胞因子(如TNF-α、IL-1β)、促进细胞衰老以及刺激异常血管生成和神经长入来加剧椎间盘退变。相比之下,抗炎M2巨噬细胞可能通过抑制炎症和增强组织修复来减轻退变。针对巨噬细胞极化的治疗策略包括药物制剂(如细胞因子、小分子抑制剂)、生物疗法、基因编辑和物理干预。挑战依然存在,如对极化触发因素理解不完整、缺乏靶向递送系统以及临床前模型中的转化成功率有限。
巨噬细胞极化是IVDD病理的关键调节因子,提供了有前景的治疗靶点。未来研究应专注于阐明极化机制、优化巨噬细胞表型的时空控制以及开发个性化疗法。应对这些挑战可能推动创新策略来阻止或逆转IVDD进展,最终改善LBP患者的临床结局。