ArticleStem cells (Dayton, Ohio)2021
Cartilage endplate stem cells inhibit intervertebral disc degeneration by releasing exosomes to nucleus pulposus cells to activate Akt/autophagy.
Article in Stem cells (Dayton, Ohio), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 papers, 1 of them a synthesis that pooled it.
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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
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Extracellular Vesicles as an Emerging Treatment Option for Intervertebral Disc Degeneration: Therapeutic Potential, Translational Pathways, and Regulatory Considerations.Advanced healthcare materials · 2022Pooled it
- Targeting Inflammatory Cell Death: A Strategy for Discogenic Pain Relief.Journal of pain research · 2026Review
- Role of Exosomes from Nucleus Pulposus Cells in Attenuating Intervertebral Disc Degeneration by Inhibiting Nucleus Pulposus Cell Apoptosis via the miR-8485/GSK-3β/Wnt/β-catenin Signaling Axis.Current molecular medicine · 2026Article
- Rim enhancement on MRI predicts long-term outcomes in extruded/migrated lumbar disc herniation managed with an inflammation-preserving protocol: a 6-year prospective cohort study.Frontiers in medicine · 2026Article
- Natural products targeting programmed cell death: a novel therapeutic strategy for intervertebral disc degeneration.International journal of surgery (London, England) · 2026Review
- Mechanobiology of intervertebral disc degeneration: From pathological mechanisms to therapeutic approaches.Mechanobiology in medicine · 2025Review
- Article
- m6A-mediated silencing of RNF41 by METTL3/YTHDC1 disrupts autophagy to drive intervertebral disc degeneration.Cell biology and toxicology · 2025Article
- Exosome Therapy: A Promising Avenue for Treating Intervertebral Disc Degeneration.Tissue engineering and regenerative medicine · 2025Review
- Quantitative assessment of lumbar intervertebral disc degeneration and its correlation with clinical symptoms: a study utilizing ultrashort time-of-echo and T2 mapping as biomarkers.BMC musculoskeletal disorders · 2025Article
- Myricetin Restores Autophagy to Attenuate Lumbar Intervertebral Disk Degeneration Via Negative Regulation of the JAK2/STAT3 Pathway.Biochemical genetics · 2025Article
- Exploring extracellular vesicles as novel therapeutic agents for intervertebral disc degeneration: delivery, applications, and mechanisms.Stem cell research & therapy · 2025Review
- Stem cell therapy for intervertebral disc degeneration: Clinical progress with exosomes and gene vectors.World journal of stem cells · 2025Review
- [Mechanism of extracellular vesicles in the repair of intervertebral disc degeneration].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2025Review
- Review
- Ferroptosis: A New Direction in the Treatment of Intervertebral Disc Degeneration.Cell biochemistry and biophysics · 2025Review
- Autophagy activation alleviates annulus fibrosus degeneration via the miR-2355-5p/mTOR pathway.Journal of orthopaedic surgery and research · 2025Article
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- Lumbar disc herniation reabsorption: a review of clinical manifestations, mechanisms, and conservative treatments.Frontiers in medicine · 2025Review
- MicroRNAs regulating apoptosis and delivery strategies for treating intervertebral disc degeneration.Frontiers in cell and developmental biology · 2025Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedErratum.2021
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Degeneration of the cartilage endplate (CEP) induces intervertebral disc degeneration (IVDD). Nucleus pulposus cell (NPC) apoptosis is also an important exacerbating factor in IVDD, but the cascade mechanism in IVDD is not clear. We investigated the apoptosis of NPCs and IVDD when stimulated by normal cartilage endplate stem cell (CESC)-derived exosomes (N-Exos) and degenerated CESC-derived exosomes (D-Exos) in vitro and in vivo. Tert-butyl hydroperoxide (TBHP) was used to induce inflammation of CESCs. The bioinformatics differences between N-Exos and D-Exos were analyzed using mass spectrometry, heat map, and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. NPC apoptosis was examined using TUNEL staining. The involvement of the AKT and autophagy signaling pathways was investigated using the signaling inhibitor LY294002. Magnetic resonance imaging, Western blotting, and immunofluorescence staining were used to evaluate the therapeutic effects of N-Exos in rats with IVDD. TBHP effectively induced inflammation and the degeneration of CEP in rat. N-Exos were more conducive to autophagy activation than D-Exos. The apoptotic rate of NPCs decreased obviously after treatment with N-Exos compared to D-Exos. N-Exos inhibited NPCs apoptosis and attenuated IVDD in rat via activation of the AKT and autophagy pathways. These results are the first findings to confirm that CEP delayed the progression of IVDD via exosomes. The therapeutic effects of N-Exos on NPC apoptosis inhibition and the slowing of IVDD progression were more effective than D-Exos due to activation of the PI3K/AKT/autophagy pathway, which explained the increase in the incidence of IVDD after inflammation of the CEP.
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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.