Cellular senescence in intervertebral disc aging and degeneration.
Cellular senescence in intervertebral disc aging and degeneration.
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DOI：
10.1007/s40610-018-0108-8
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发表时间：
2018-12
期刊：
影响因子：
--
通讯作者：
Vo N
中科院分区：
文献类型：
--
作者：
Patil P;Niedernhofer LJ;Robbins PD;Lee J;Sowa G;Vo N
年龄是多种疾病病理的主要风险因素，包括慢性背痛，其源于椎间盘组织的年龄相关退行性变化。越来越多的证据表明，椎间盘细胞表型向衰老表型的变化可能是年龄相关性椎间盘退变的主要驱动力之一。这篇综述讨论了已知的压力，促进椎间盘组织和潜在的分子机制，椎间盘细胞通过衰老表型的转变，使其发展。随着年龄的增长和椎间盘组织的退变，衰老细胞的数量增加。此外，体外研究已经证实了应激诱导的衰老椎间盘细胞的分解代谢性质。已经显示出几种因素通过多种不同的潜在机制建立衰老。细胞衰老可以作为治疗靶点来对抗年龄相关的椎间盘退变。然而，是否不同的压力，利用不同的信号网络建立不同类型的椎间盘细胞的衰老类型是目前未知的，值得进一步研究。
Age is a major risk factor for multiple disease pathologies, including chronic back pain, which stems from age-related degenerative changes to intervertebral disc tissue. Growing evidence suggest that the change in phenotype of disc cells to a senescent phenotype may be one of the major driving forces of age-associated disc degeneration. This review discusses the known stressors that promote development of senescence in disc tissue and the underlying molecular mechanisms disc cells adopt to enable their transition to a senescent phenotype. Increased number of senescent cells have been observed with advancing age and degeneration in disc tissue. Additionally, in vitro studies have confirmed the catabolic nature of stress-induced senescent disc cells. Several factors have been shown to establish senescence via multiple different underlying mechanisms. Cellular senescence can serve as a therapeutic target to combat age-associated disc degeneration. However, whether the different stressors utilizing different signaling networks establish different kinds of senescent types in disc cells is currently unknown and warrants further investigation.