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.

中文翻译：

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细胞衰老：椎间盘退变病理中生存压力下不可忽略的细胞状态。

随着年龄的增长，椎间盘退变（IDD）主要表现为腰背痛（LBP），伴有身体机能的丧失。这些病理过程可以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，并使变性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密切相关。这些联系的越来越多的证据要求我们收集从潜在危险因素到发病机理的关键线索，以及用于延迟细胞衰老和减轻变性变化的相关干预措施。在本文中，我们试图阐明IDD中除细胞死亡以外的另一个重要细胞状态，并讨论细胞和细胞外微环境的衰老相关变化。然后，我们强调氧化应激和表观基因组扰动在IDD发作中将危险因素与细胞衰老联系起来的作用。此外，我们总结了针对衰老细胞的当前干预措施，这些干预措施可能会在IDD中发挥抗变性的作用。