ArticleInternational orthopaedics2014
Accelerated premature stress-induced senescence of young annulus fibrosus cells of rats by high glucose-induced oxidative stress.
Article in International orthopaedics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Pooled it
- PI3KCD gene expression and its role in diabetic intervertebral disc degeneration running title: PI3KCD gene crucial for diabetic IDH.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Adapt, Mitigate, and Target: The Role of Oxidative Stress in Intervertebral Disc Homeostasis and Disc Degeneration.Neurospine · 2026Review
- Cellular and molecular mechanisms of diabetes-mediated disc degeneration.Frontiers in endocrinology · 2026Review
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
- Risk factors for recurrent lumbar disc herniation after unilateral biportal endoscopy: a retrospective study.International orthopaedics · 2025Article
- Exploring the Causes of Intervertebral Disc Annulus Fibrosus Impairment.Cellular and molecular bioengineering · 2025Review
- BMAL1 attenuates intervertebral disc degeneration by activating the SIRT1/PGC-1α pathway: evidence from vitro studies.Scientific reports · 2025Article
- NRF2 in age-related musculoskeletal diseases: Role and treatment prospects.Genes & diseases · 2024Review
- Phillyrin reduces ROS production to alleviate the progression of intervertebral disc degeneration by inhibiting NF-κB pathway.Journal of orthopaedic surgery and research · 2024Article
- From hyperglycemia to intervertebral disc damage: exploring diabetic-induced disc degeneration.Frontiers in immunology · 2024Review
- Machine learning algorithm predicts fibrosis-related blood diagnosis markers of intervertebral disc degeneration.BMC medical genomics · 2023Article
- Review
- Oxidative stress in intervertebral disc degeneration: Molecular mechanisms, pathogenesis and treatment.Cell proliferation · 2023Review
- Intervertebral disc cell fate during aging and degeneration: apoptosis, senescence, and autophagy.North American Spine Society journal · 2023Article
- Cellular Senescence in Intervertebral Disc Aging and Degeneration: Molecular Mechanisms and Potential Therapeutic Opportunities.Biomolecules · 2023Review
- Strong association of lumbar disk herniation with diabetes mellitus: a 12-year nationwide retrospective cohort study.Frontiers in endocrinology · 2023Article
- The Nrf2 antioxidant defense system in intervertebral disc degeneration: Molecular insights.Experimental & molecular medicine · 2022Review
- Diabetes Mellitus and the Development of Lumbar Canal Stenosis: Is There Any Relevance?Asian spine journal · 2022Article
- Diabetes Mellitus-A Risk Factor for the Development of Lumbar Disc Degeneration: A Retrospective Study of an Indian Population.Global spine journal · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposesDiabetes mellitus (DM) is thought to be an important aetiological factor in intervertebral disc degeneration. A glucose-mediated increase of oxidative stress is a major causative factor in development of diseases associated with DM. The aim of this study was to investigate the effect of high glucose on mitochondrial damage, oxidative stress and senescence of young annulus fibrosus (AF) cells.
methodsAF cells were isolated from four-week-old young rats, cultured, and placed in either 10 % FBS (normal control) or 10 % FBS plus two different high glucose concentrations (0.1 M and 0.2 M) (experimental conditions) for one and three days. We identified and quantified the mitochondrial damage and reactive oxygen species (ROS) (oxidative stress). We also identified and quantified the occurrence of senescence and telomerase activity. Finally, the expressions of proteins were determined related to replicative senescence (p53-p21-pRB) and stress-induced senescence (p16-pRB).
resultsTwo high glucoses enhanced the mitochondrial damage in young rat AF cells, which resulted in an excessive generation of ROS in a dose- and time-dependent manner for one and three days compared to normal control. Two high glucose concentrations increased the occurrence of senescence of young AF cells in a dose- and time-dependent manner. Telomerase activity declined in a dose- and time-dependent manner. Both high glucose treatments increased the expressions of p16 and pRB proteins in young rat AF cells for one and three days. However, compared to normal control, the expressions of p53 and p21 proteins were decreased in young rat AF cells treated with both high glucoses for one and three days.
conclusionsThe present study demonstrated that high glucose-induced oxidative stress accelerates premature stress-induced senescence in young rat AF cells in a dose- and time-dependent manner rather than replicative senescence. These results suggest that prevention of excessive generation of oxidative stress by strict blood glucose control could be important to prevent or to delay premature intervertebral disc degeneration in young patients with DM.
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.