ROS: Crucial Intermediators in the Pathogenesis of Intervertebral Disc Degeneration
Open accessAbstract
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.
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ROS can lead to the loss of nucleus pulposus cells or diminish their functionality, resulting in an imbalance between anabolic and catabolic processes of the extracellular matrix characteristic of intervertebral disc degeneration.
“Prior studies have shown that ROS can lead to the loss of NP cells or diminish their functionality, resulting in an imbalance between the anabolic and catabolic processes of the extracellular matrix (ECM), which is characteristic of IDD47.”
From ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis (2025) · cites this paper as [47]
ROS accumulation is an important stimulator for NF-κB signal activation.
“ROS accumulation is an important stimulatory for NF-κB signal activation47–49”
From ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis (2025) · cites this paper as [47]
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Cited by
Sorted by citations
Chen, Z., Zhao, C., Liu, P., Huang, H., Zhang, S., & Wang, X. (2021) · CARTILAGE · doi:10.1177/19476035211038748 · Cited by 42 · see citing works
ATF1 and miR-27b-3p drive intervertebral disc degeneration through the PPARG/NF-κB signaling axis
Guo, W., Mu, K., Geng, J.-C., Xing, H.-Y., Dong, Y., Liu, W.-D., Wang, S.-C., Shi, J.-X., Xing, B.-R., Zhao, J.-Y., et al. (2025) · Communications Biology · doi:10.1038/s42003-025-08186-6 · Cited by 7 · see citing works
- Authors
- Feng, C., Yang, M., Lan, M., Liu, C., Zhang, Y., Huang, B., Liu, H., & Zhou, Y.
- Affiliations
- Army Medical University (CN)
- Corresponding author
- Liu, Huan
- Zhou, Yue
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2017-01
- Volume
- 2017
- Issue
- 1
- Pages
- 5601593-5601593
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC5368368
- OpenAlex
- W2603552684
- Cited by
- 384
- References
- 6
- Citations by year
- 2026: 34 · 2025: 44 · 2024: 48 · 2023: 60 · 2022: 77 · 2021: 51 · 2020: 27 · 2019: 25 · 2018: 15 · 2017: 3
- FWCI
- 3.06
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81572186, 81271982, 81472076, 81401801)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spine and Intervertebral Disc Pathology
- Health Sciences › Medicine › Surgery › Cervical and Thoracic Myelopathy
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Keywords
- intervertebral disc degeneration, reactive oxygen species, oxidative stress, matrix degradation, inflammation, apoptosis, autophagy, cellular senescence, antioxidant supplementation
- MeSH terms
- Homeostasis, Humans, Intervertebral Disc, Oxidation-Reduction, Reactive Oxygen Species, Intervertebral Disc Degeneration, Cellular Microenvironment
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