Wang Feng, Zheng Chenjingmei, Wu Xiaotao
Department of Orthopaedics, Affiliated Zhongda Hospital of Southeast University, Nanjing Jiangsu, 210009, P.R.China.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2012 Dec;26(12):1448-52.
To summarize the role of cellular senescence and senescent secretary phenotype in the intervertebral disc (IVD) degeneration.
Relevant articles that discussed the roles of cellular senescence in the IVD degeneration were extensively reviewed, and retrospective and comprehensive analysis was performed. The senescent phenomenon during IVD degeneration, senescent secretary phenotype of the disc cells, senescent pathways within the IVD microenvironment, as well as the anti-senescent approaches for IVD regeneration were systematically reviewed.
During aging and degeneration, IVD cells gradually and/or prematurely undergo senescence by activating p53-p21-retinoblastoma (RB) or p161NK4A-RB senescent pathways. The accumulation of senescent cells not only decreases the self-renewal ability of IVD, but also deteriorates the disc microenvironment by producing more inflammatory cytokines and matrix degrading enzymes. More specific senescent biomarkers are required to fully understand the phenotype change of senescent disc cells during IVD degeneration. Molecular analysis of the senescent disc cells and their intracellular signaling pathways are needed to get a safer and more efficient anti-senescence strategy for IVD regeneration.
Cellular senescence is an important mechanism by which IVD cells decrease viability and degenerate biological behaviors, which provide a new thinking to understand the pathogenesis of IVD degeneration.
总结细胞衰老和衰老相关分泌表型在椎间盘退变中的作用。
广泛回顾讨论细胞衰老在椎间盘退变中作用的相关文章,并进行回顾性综合分析。系统综述椎间盘退变过程中的衰老现象、椎间盘细胞的衰老相关分泌表型、椎间盘微环境中的衰老途径以及椎间盘再生的抗衰老方法。
在衰老和退变过程中,椎间盘细胞通过激活p53-p21-视网膜母细胞瘤(RB)或p161NK4A-RB衰老途径逐渐和/或过早地发生衰老。衰老细胞的积累不仅降低了椎间盘的自我更新能力,还通过产生更多的炎性细胞因子和基质降解酶使椎间盘微环境恶化。需要更特异的衰老生物标志物来全面了解椎间盘退变过程中衰老椎间盘细胞的表型变化。需要对衰老椎间盘细胞及其细胞内信号通路进行分子分析,以获得更安全、更有效的椎间盘再生抗衰老策略。
细胞衰老是椎间盘细胞活力下降和生物学行为退变的重要机制,为理解椎间盘退变的发病机制提供了新的思路。