椎间盘细胞衰老的分子机制:端粒、线粒体与细胞代谢重编程
邓威1,2, 朱若辰1,2, 孔凡国3, 栾继耀1,3,*
1广州中医药大学,广州 510006;2广州中医药大学第一临床医学院/广州中医药大学附属第一医院脊柱微创科,广州 510006;3河南省洛阳正骨医院/河南省骨科医院脊柱微创外二科,郑州 450000
摘要
椎间盘退变(intervertebral disc degeneration, IVDD)作为常见脊柱疾病,其发病机制与椎间盘细胞衰老密切相关。细胞衰老导致椎间盘生物力学特性改变,并引起慢性疼痛和功能障碍等临床症状。当前研究表明,端粒缩短、线粒体功能障碍和细胞代谢重编程构成椎间盘细胞衰老的核心分子机制。本文系统综述椎间盘细胞衰老的分子机制,分析端粒动力学、线粒体稳态失衡及代谢重编程在此过程中的作用,并总结相应的潜在治疗策略。通过阐明这些分子机制,为开发延缓IVDD的治疗靶点提供理论基础。
关键词: 椎间盘退变; 细胞衰老; 端粒; 线粒体; 代谢重编程
Molecular mechanism of intervertebral disc cell senescence: telomeres, mitochondria, and cellular metabolic reprogramming
DENG Wei1,2, ZHU Ruo-Chen1,2, KONG Fan-Guo3, LUAN Ji-Yao1,3,*
1Guangzhou University of Chinese Medicine, Guangzhou 510006, China;2Department of Minimally Invasive Spine Surgery, The First Clinical Medical College of Guangzhou University of Chinese Medicine/The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510006, China;3The Second Department of Minimally Invasive Spine Surgery, Luoyang Orthopedic Hospital of Henan Province/Orthopedic Hospital of Henan Province, Zhengzhou 450000, China
Abstract
Intervertebral disc degeneration (IVDD), as a common spinal disorder, is closely associated with intervertebral disc cell senescence in its pathogenesis. Cellular senescence leads to alterations in the biomechanical properties of intervertebral discs and causes clinical symptoms including chronic pain and functional impairment. Current research demonstrates that telomere shortening, mitochondrial dysfunction, and cellular metabolic reprogramming constitute the core molecular mechanisms underlying intervertebral disc cell senescence. This review systematically examines the molecular mechanisms of intervertebral disc cell senescence, analyzes the roles of telomere dynamics, mitochondrial homeostasis imbalance, and metabolic reprogramming in this process, and summarizes corresponding potential therapeutic strategies. By elucidating these molecular mechanisms, this work provides a theoretical foundation for developing therapeutic targets to delay IVDD.
Key words: intervertebral disc degeneration; cellular senescence; telomeres; mitochondria; metabolic reprogramming
收稿日期: 录用日期:
通讯作者:栾继耀 E-mail:
DOI: 10.13294/j.aps.2026.0044
引用本文:
邓威, 朱若辰, 孔凡国, 栾继耀. 椎间盘细胞衰老的分子机制:端粒、线粒体与细胞代谢重编程[J]. 生理学报 2026; 78 (3): 566-578.
DENG Wei, ZHU Ruo-Chen, KONG Fan-Guo, LUAN Ji-Yao. Molecular mechanism of intervertebral disc cell senescence: telomeres, mitochondria, and cellular metabolic reprogramming. Acta Physiol Sin 2026; 78 (3): 566-578 (in Chinese with English abstract).