ArticleOxidative medicine and cellular longevity2017
Autophagy Is a Protective Response to the Oxidative Damage to Endplate Chondrocytes in Intervertebral Disc: Implications for the Treatment of Degenerative Lumbar Disc.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Oligosaccharide nanomedicine of alginate sodium improves therapeutic results of posterior lumbar interbody fusion with cages for degenerative lumbar disease in osteoporosis patients by downregulating serum miR-155.International journal of nanomedicine · 2017Trial
- Nano-Drug Delivery System Targeting the Oxidative Stress Microenvironment: A Prospective Strategy for Intervertebral Disc Degeneration Treatment.International journal of nanomedicine · 2025Review
- NRF2 in age-related musculoskeletal diseases: Role and treatment prospects.Genes & diseases · 2024Review
- Transcriptional profiling of human cartilage endplate cells identifies novel genes and cell clusters underlying degenerated and non-degenerated phenotypes.Arthritis research & therapy · 2024Article
- Screening and identification of microRNAs mediating cartilage endplate degeneration in human intervertebral disks.Frontiers in medicine · 2024Article
- Mechanism of the Mitogen-Activated Protein Kinases/Mammalian Target of Rapamycin Pathway in the Process of Cartilage Endplate Stem Cell Degeneration Induced by Tension Load.Global spine journal · 2023Article
- Oxidative stress in intervertebral disc degeneration: Molecular mechanisms, pathogenesis and treatment.Cell proliferation · 2023Review
- Emerging role and therapeutic implication of mTOR signalling in intervertebral disc degeneration.Cell proliferation · 2023Review
- Circular RNA and intervertebral disc degeneration: unravelling mechanisms and implications.Frontiers in molecular biosciences · 2023Review
- Orientin downregulating oxidative stress-mediated endoplasmic reticulum stress and mitochondrial dysfunction through AMPK/SIRT1 pathway in rat nucleus pulposus cells in vitro and attenuated intervertebral disc degeneration in vivo.Apoptosis : an international journal on programmed cell death · 2022Article
- Targeting Autophagy for Developing New Therapeutic Strategy in Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
- The Nrf2 antioxidant defense system in intervertebral disc degeneration: Molecular insights.Experimental & molecular medicine · 2022Review
- Novel Methods to Measure Height and Volume in Healthy and Degenerated Lumbar Discs in MRIs: A Reliability Assessment Study.Diagnostics (Basel, Switzerland) · 2022Article
- Effects and Mechanism ofBioMed research international · 2022Article
- The role of ageing and oxidative stress in intervertebral disc degeneration.Frontiers in molecular biosciences · 2022Review
- miR-142-3p and HMGB1 Are Negatively Regulated in Proliferation, Apoptosis, Migration, and Autophagy of Cartilage Endplate Cells.Cartilage · 2021Article
- AMPK as a Potential Therapeutic Target for Intervertebral Disc Degeneration.Frontiers in molecular biosciences · 2021Review
- Eicosapentaenoic Acid-Induced Autophagy Attenuates Intervertebral Disc Degeneration by Suppressing Endoplasmic Reticulum Stress, Extracellular Matrix Degradation, and Apoptosis.Frontiers in cell and developmental biology · 2021Article
- Heme Oxygenase-1-Mediated Autophagy Protects against Oxidative Damage in Rat Nucleus Pulposus-Derived Mesenchymal Stem Cells.Oxidative medicine and cellular longevity · 2020Article
- Effects of simvastatin-loaded PLGA microspheres on treatment of rats with intervertebral disk degeneration and on 6-K-PGF1α and HIF-1α.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low back pain (LBP) is the leading cause of disability in the elderly. Intervertebral disc degeneration (IDD) was considered as the main cause for LBP. Degeneration of cartilaginous endplate was a crucial harmful factor during the initiation and development of IDD. Oxidative stress was implicated in IDD. However, the underlying molecular mechanism for the degeneration of cartilaginous endplate remains elusive. Herein, we found that oxidative stress could induce apoptosis and autophagy in endplate chondrocytes evidenced by western blot analysis, flow cytometry, immunofluorescence staining, GFP-LC3B transfection, and MDC staining. In addition, we also found that the apoptosis of endplate chondrocytes was significantly increased after the inhibition of autophagy by bafilomycin A1 shown by flow cytometry. Furthermore, mTOR pathway upstream autophagy was greatly suppressed suggested by western blot assay. In conclusion, our study strongly revealed that oxidative stress could increase autophagy and apoptosis of endplate chondrocytes in intervertebral disc. The increase of autophagy activity could prevent endplate chondrocytes from apoptosis. The autophagy in endplate chondrocytes induced by oxidative stress was mTOR dependent. These findings might shed some new lights on the mechanism for IDD and provide new strategies for the treatments of IDD.
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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.