ReviewFrontiers in molecular biosciences2022
The role of ageing and oxidative stress in intervertebral disc degeneration.
Review in Frontiers in molecular biosciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- Intradiscal Delivery of Notoginsenoside R1-Loaded PLGA Nanoparticles Attenuates Intervertebral Disc Degeneration in Rats.Journal of cellular and molecular medicine · 2026Article
- Superoxide dismutase in intervertebral disc degeneration: from pathophysiological mechanism to therapeutic strategies.Molecular biology reports · 2026Review
- Article
- Proteomic analysis identifies distinct signaling pathways in lumbar intervertebral disc degeneration between type-2 diabetic and non-diabetic patients.Scientific reports · 2026Article
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Cellular and molecular mechanisms of diabetes-mediated disc degeneration.Frontiers in endocrinology · 2026Review
- Blood and lymphatic vascular remodeling in intervertebral disc degeneration.Frontiers in immunology · 2026Review
- TAFA4 Mitigates Intervertebral Disc Degeneration by Modulating Macrophage Polarization and Inhibiting ROS-NLRP3 Inflammasome Activation.Neurospine · 2026Article
- Etiology, diagnosis and treatment of lumbar disc degeneration: a focus on the mechanism of action of Piezo1 and research perspectives.Frontiers in cell and developmental biology · 2026Review
- Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025Review
- Construction of a novel 3-gene diagnostic signature related to senescence in intervertebral disc degeneration.European journal of medical research · 2025Article
- ROS-degradable hydrogel delivering LOXL2-LNPs rescues disc degeneration by synchronously suppressing cellular senescence and oxidative damage.Journal of nanobiotechnology · 2025Article
- Cuttlefish ink nanoparticle-engineered hydrogel microspheres synergistically attenuate disc degeneration via antioxidant defense and matrix synthesis activation.Materials today. Bio · 2025Article
- Pure platelet-rich plasma delays intervertebral disc degeneration by activating SIRT1-mediated autophagy in nucleus pulposus cells.Journal of orthopaedic surgery and research · 2025Article
- Novel anti-pyroptosis drug loaded on metal-organic framework for intervertebral disc degeneration therapy.Materials today. Bio · 2025Article
- MOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration.Materials today. Bio · 2025Article
- 1,25(OH)₂D₃ inhibits ferroptosis in nucleus pulposus cells via VDR signaling to mitigate lumbar intervertebral disc degeneration.Scientific reports · 2025Article
- Article
- The Significance of MAPK Signaling Pathway in the Diagnosis and Subtype Classification of Intervertebral Disc Degeneration.JOR spine · 2025Article
- Human molecular mechanisms of discogenic low back pain: A scoping review.The journal of pain · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) is the primary cause of intervertebral disc (IVD) disease. With the increased ageing of society, an increasing number of patients are plagued by intervertebral disc disease. Ageing not only accelerates the decreased vitality and functional loss of intervertebral disc cells but also increases intracellular oxidative stress. Moreover, the speed of intervertebral disc ageing is also linked to high levels of reactive oxygen species (ROS) production. Not only is the production of ROS increased in ageing intervertebral disc cells, but antioxidant levels in degenerative intervertebral discs also decrease. In addition to the intervertebral disc, the structural components of the intervertebral disc matrix are vulnerable to oxidative damage. After chronic mitochondrial dysfunction, ROS can be produced in large quantities, while autophagy can eliminate these impaired mitochondria to reduce the production of ROS. Oxidative stress has a marked impact on the occurrence of IDD. In the future, IDD treatment is aiming to improve oxidative stress by regulating the redox balance in intervertebral disc cells. In summary, ageing and oxidative stress promote the degeneration of IVD, but further basic and clinical trials are needed to determine how to treat oxidative stress. At present, although there are many in-depth studies on the relationship between oxidative stress and degeneration of intervertebral disc cells, the specific mechanism has not been elucidated. In this paper, the main causes of intervertebral disc diseases are studied and summarized, and the impact of oxidative stress on intervertebral disc degeneration is studied.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.