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氧化应激在椎间盘退变中的作用:机制、发病机制及治疗策略

Role of oxidative stress in intervertebral disc degeneration: mechanisms, pathogenesis, and therapeutic strategies.

作者信息

Zhang Cong, Li Cheng-Ming, Jiang Qing

机构信息

Division of Sports Medicine and Adult Reconstructive Surgery, Department of Orthopedic Surgery, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, Nanjing, 210008, Jiangsu, PR China.

Department of Spine Surgery, School of Medicine, Zhongda Hospital, Southeast University, Nanjing, 210008, Jiangsu, PR China.

出版信息

Mol Biol Rep. 2025 May 2;52(1):444. doi: 10.1007/s11033-025-10538-8.

Abstract

Intervertebral disc degeneration (IDD) is a prevalent and debilitating spinal condition, characterised by the progressive degradation of disc structure and function, often accompanied by pain. Despite our increasing understanding of IDD, the precise mechanisms underlying its development and potential therapeutic targets remain incompletely understood. Recent research has highlighted that oxidative stress, along with immune abnormalities, mechanical loading imbalances, and metabolic disruptions, play a pivotal role in IDD initiation and progression. Oxidative stress in IDD results from an overproduction of reactive oxygen species (ROS) and a compromised ability to eliminate them, disrupting the redox homeostasis within the intervertebral disc. This disturbance in redox balance leads to extracellular matrix degradation (ECM), induces cellular apoptosis, and worsens the damage to disc tissues. This review provides a comprehensive overview of the pathophysiological processes of IDD, with a particular focus on the role of oxidative stress. Additionally, we explore current advancements in therapeutic strategies targeting oxidative stress, including antioxidant drugs, biomaterials, and stem cell-based approaches, offering promising avenues for the management and treatment of IDD.

摘要

椎间盘退变(IDD)是一种常见且使人衰弱的脊柱疾病,其特征是椎间盘结构和功能逐渐退化,常伴有疼痛。尽管我们对IDD的认识不断增加,但其发展的精确机制和潜在治疗靶点仍未完全了解。最近的研究强调,氧化应激与免疫异常、机械负荷失衡和代谢紊乱一起,在IDD的起始和进展中起关键作用。IDD中的氧化应激是由于活性氧(ROS)产生过多以及清除它们的能力受损,从而破坏了椎间盘内的氧化还原稳态。这种氧化还原平衡的紊乱导致细胞外基质降解(ECM),诱导细胞凋亡,并加剧对椎间盘组织的损伤。本综述全面概述了IDD的病理生理过程,特别关注氧化应激的作用。此外,我们探讨了针对氧化应激的治疗策略的当前进展,包括抗氧化药物、生物材料和基于干细胞的方法,为IDD的管理和治疗提供了有希望的途径。

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