椎间盘细胞的氧化应激损伤在椎间盘退变机制中的研究进展

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摘要椎间盘是人体最大的无血管组织，由中央的髓核(nucleus pulposus，NP)、外周的纤维环(annulus fibrosus，AF)及软骨终板(cartilage endplate，CEP)三部分组成。椎间盘细胞主要通过CEP以扩散的方式来吸收营养物质及排出代谢产物，因此椎间盘细胞分裂不活跃、修复能力差是造成椎间盘退变(intervertebral disc degeneration，IVDD)的潜在原因。
IVDD是指椎间盘自然退变和衰老的生理病理过程，是临床各种脊柱退变性疾病的基础。IVDD常导致脊柱不稳、椎间盘突出和椎管狭窄，从而出现腰痛伴有或不伴有神经根或脊髓压迫症状，极大地影响患者的生活质量。目前，多项研究表明细胞外基质降解、炎症反应、氧化应激、线粒体功能障碍、端粒缩短和DNA损伤、营养剥夺、异常机械负荷和表观遗传改变等病理因素参与IVDD的进展，其中氧化应激损伤是主要机制之一，可能通过多个途径影响椎间盘细胞。

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	宰爽嘉1
	张亮1*
	李争光1
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	吴火峰1
	孙华1
	张永博1
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	陈浏阳1
	戴睿1
	张志强1

基金资助:国家自然科学基金面上项目(82172462)；江苏省中医药科技发展计划项目(YB2020085/MS2021079)；苏北人民医院院级科研基金(交叉合作专项)(SBJC21014)

通讯作者: 张亮

作者简介: 宰爽嘉(1999－ )，男，研究生在读，〖JP3〗江苏省苏北人民医院，扬州大学附属苏北人民医院脊柱骨科，zaishuangjia@163.com

引用本文:

宰爽嘉1，张亮1*，李争光1，2，吴火峰1，孙华1，张永博1，3，陈浏阳1，戴睿1，张志强1. 椎间盘细胞的氧化应激损伤在椎间盘退变机制中的研究进展[J]. 实用骨科杂志, 2024, 30(7): 621-.

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http://www.sygkzz.com/CN/ 或 http://www.sygkzz.com/CN/Y2024/V30/I7/621

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