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活性氧:椎间盘退变发病机制中的关键介质

ROS: Crucial Intermediators in the Pathogenesis of Intervertebral Disc Degeneration.

作者信息

Feng Chencheng, Yang Minghui, Lan Minghong, Liu Chang, Zhang Yang, Huang Bo, Liu Huan, Zhou Yue

机构信息

Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.

出版信息

Oxid Med Cell Longev. 2017;2017:5601593. doi: 10.1155/2017/5601593. Epub 2017 Mar 14.

DOI:10.1155/2017/5601593
PMID:28392887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5368368/
Abstract

Excessive reactive oxygen species (ROS) generation in degenerative intervertebral disc (IVD) indicates the contribution of oxidative stress to IVD degeneration (IDD), giving a novel insight into the pathogenesis of IDD. ROS are crucial intermediators in the signaling network of disc cells. They regulate the matrix metabolism, proinflammatory phenotype, apoptosis, autophagy, and senescence of disc cells. Oxidative stress not only reinforces matrix degradation and inflammation, but also promotes the decrease in the number of viable and functional cells in the microenvironment of IVDs. Moreover, ROS modify matrix proteins in IVDs to cause oxidative damage of disc extracellular matrix, impairing the mechanical function of IVDs. Consequently, the progression of IDD is accelerated. Therefore, a therapeutic strategy targeting oxidative stress would provide a novel perspective for IDD treatment. Various antioxidants have been proposed as effective drugs for IDD treatment. Antioxidant supplementation suppresses ROS production in disc cells to promote the matrix synthesis of disc cells and to prevent disc cells from death and senescence in vitro. However, there is not enough in vivo evidence to support the efficiency of antioxidant supplementation to retard the process of IDD. Further investigations based on in vivo and clinical studies will be required to develop effective antioxidative therapies for IDD.

摘要

在退变的椎间盘(IVD)中,活性氧(ROS)过度生成表明氧化应激对椎间盘退变(IDD)有影响,这为IDD的发病机制提供了新的见解。ROS是椎间盘细胞信号网络中的关键介质。它们调节椎间盘细胞的基质代谢、促炎表型、凋亡、自噬和衰老。氧化应激不仅增强基质降解和炎症,还促进IVD微环境中存活且有功能的细胞数量减少。此外,ROS会修饰IVD中的基质蛋白,导致椎间盘细胞外基质的氧化损伤,损害IVD的力学功能。因此,IDD的进展会加速。所以,针对氧化应激的治疗策略将为IDD治疗提供新的视角。各种抗氧化剂已被提议作为治疗IDD的有效药物。补充抗氧化剂可抑制椎间盘细胞中ROS的产生,以促进椎间盘细胞的基质合成,并在体外防止椎间盘细胞死亡和衰老。然而,尚无足够的体内证据支持补充抗氧化剂可延缓IDD进程的有效性。需要基于体内和临床研究进行进一步调查,以开发针对IDD的有效抗氧化疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/382f6cde809c/OMCL2017-5601593.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/139ee7001685/OMCL2017-5601593.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/b5d7a3dc6413/OMCL2017-5601593.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/382f6cde809c/OMCL2017-5601593.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/139ee7001685/OMCL2017-5601593.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/b5d7a3dc6413/OMCL2017-5601593.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c473/5368368/382f6cde809c/OMCL2017-5601593.003.jpg

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2
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3
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4
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