Chen Heng, Tang Tian, Xue Congyang, Liu Xin, Xi Zhipeng, Xie Lin, Kang Ran
Affiliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210028, China.
Nanjing University of Chinese Medicine, Nanjing, 210028, China.
J Orthop Surg Res. 2024 Dec 5;19(1):825. doi: 10.1186/s13018-024-05280-z.
Low back pain caused by intervertebral disc degeneration (IDD) has emerged as a significant global public health concern, with far-reaching consequences for patients' quality of life and healthcare systems. Although previous research have revealed that the mechanisms of intervertebral disc cell apoptosis, pyroptosis and necroptosis can aggravate IDD damage by mediating inflammation and promoting extracellular matrix degradation, but they cannot explain the connection between different cell death mechanisms and ion metabolism disorders. The latest study shows that cell death mechanisms such as cellular senescence, ferroptosis, and cuproptosis, and PANopotosis have similar roles in the progression of intervertebral disc degeneration, but not exactly the same damage mechanism. This paper summarizes the effects of various cell death patterns on the disease progression of IDD, related molecular mechanisms and signaling pathways, providing new perspectives and potential clinical intervention strategies for the prevention and treatment of IDD.
由椎间盘退变(IDD)引起的腰痛已成为一个重大的全球公共卫生问题,对患者的生活质量和医疗系统产生深远影响。尽管先前的研究表明,椎间盘细胞凋亡、焦亡和坏死性凋亡机制可通过介导炎症和促进细胞外基质降解来加重IDD损伤,但它们无法解释不同细胞死亡机制与离子代谢紊乱之间的联系。最新研究表明,细胞衰老、铁死亡、铜死亡和PANoptosis等细胞死亡机制在椎间盘退变进展中具有相似作用,但损伤机制并不完全相同。本文总结了各种细胞死亡模式对IDD疾病进展的影响、相关分子机制和信号通路,为IDD的预防和治疗提供了新的视角和潜在的临床干预策略。