The Role of Oxidative Stress in Intervertebral Disc Degeneration

Author:

Cao Guoshuai1ORCID,Yang Sidong2ORCID,Cao Jianye3ORCID,Tan Zixuan3ORCID,Wu Linyu3ORCID,Dong Fang4ORCID,Ding Wenyuan2ORCID,Zhang Feng3ORCID

Affiliation:

1. Department of Clinical Medicine, Hebei Medical University, Shijiazhuang 050051, China

2. Department of Spine Surgery, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China

3. Department of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China

4. Department of Clinical Laboratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China

Abstract

Intervertebral disc degeneration is a very common type of degenerative disease causing severe socioeconomic impact, as well as a major cause of discogenic low back pain and herniated discs, placing a heavy burden on patients and the clinicians who treat them. IDD is known to be associating with a complex process involving in extracellular matrix and cellular damage, and in recent years, there is increasing evidence that oxidative stress is an important activation mechanism of IDD and that reactive oxygen and reactive nitrogen species regulate matrix metabolism, proinflammatory phenotype, autophagy and senescence in intervertebral disc cells, apoptosis, autophagy, and senescence. Despite the tremendous efforts of researchers within the field of IDD pathogenesis, the proven strategies to prevent and treat this disease are still very limited. Up to now, several antioxidants have been proved to be effective for alleviating IDD. In this article, we discussed that oxidative stress accelerates disc degeneration by influencing aging, inflammation, autophagy, and DNA methylation, and summarize some antioxidant therapeutic measures for IDD, indicating that antioxidant therapy for disc degeneration holds excellent promise.

Funder

Natural Science Foundation of Hebei Province

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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