Zhang Yuang, Yang Biao, Wang Jingkai, Cheng Feng, Shi Kesi, Ying Liwei, Wang Chenggui, Xia Kaishun, Huang Xianpeng, Gong Zhe, Yu Chao, Li Fangcai, Liang Chengzhen, Chen Qixin
Department of Orthopedics Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, 310009 Hangzhou, Zhejiang, China.
Zhejiang Key Laboratory of Bone and Joint Precision and Department of Orthopedics Research Institute of Zhejiang University, Hangzhou, Zhejiang 310009, China.
Oxid Med Cell Longev. 2020 Aug 31;2020:9503562. doi: 10.1155/2020/9503562. eCollection 2020.
The intervertebral disc degeneration (IDD) with increasing aging mainly manifests as low back pain (LBP) accompanied with a loss of physical ability. These pathological processes can be preliminarily interpreted as a series of changes at cellular level. In addition to cell death, disc cells enter into the stagnation with dysfunction and deteriorate tissue microenvironment in degenerative discs, which is recognized as cell senescence. During aging, many intrinsic and extrinsic factors have been proved to have strong connections with these cellular senescence phenomena. Growing evidences of these connections require us to gather up critical cues from potential risk factors to pathogenesis and relative interventions for retarding cell senescence and attenuating degenerative changes. In this paper, we try to clarify another important cell state apart from cell death in IDD and discuss senescence-associated changes in cells and extracellular microenvironment. Then, we emphasize the role of oxidative stress and epigenomic perturbations in linking risk factors to cell senescence in the onset of IDD. Further, we summarize the current interventions targeting senescent cells that may exert the benefits of antidegeneration in IDD.
随着年龄增长,椎间盘退变(IDD)主要表现为下腰痛(LBP)并伴有身体机能丧失。这些病理过程可初步解释为细胞水平的一系列变化。除细胞死亡外,椎间盘细胞进入功能障碍的停滞状态,并使退变椎间盘中的组织微环境恶化,这被认为是细胞衰老。在衰老过程中,许多内在和外在因素已被证明与这些细胞衰老现象有密切联系。这些联系的证据越来越多,要求我们从潜在风险因素中收集关键线索,以了解发病机制以及延缓细胞衰老和减轻退变变化的相关干预措施。在本文中,我们试图阐明IDD中除细胞死亡之外的另一种重要细胞状态,并讨论细胞和细胞外微环境中与衰老相关的变化。然后,我们强调氧化应激和表观基因组扰动在将风险因素与IDD发病过程中的细胞衰老联系起来的作用。此外,我们总结了目前针对衰老细胞的干预措施,这些措施可能在IDD中发挥抗退变的益处。