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Molecular mechanism of intervertebral disc cell senescence: telomeres, mitochondria, and cellular metabolic reprogramming

DENG Wei^1,2, ZHU Ruo-Chen^1,2, KONG Fan-Guo³, LUAN Ji-Yao^1,3,*

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

Received: 　　Accepted:

Corresponding author: 栾继耀　　E-mail:

DOI: 10.13294/j.aps.2026.0044

Citing This Article：

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).