ReviewJOR spine2025
Mechanistic Interactions Driving Nucleus Pulposus Cell Senescence in Intervertebral Disc Degeneration: A Multi-Axial Perspective of Mechanical, Immune, and Metabolic Pathways.
Review in JOR spine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed.
- CBX3 aggravates nucleus pulposus cell apoptosis and extracellular matrix degradation in vitro via repressing SESN2-mediated mitophagy in an H3K9me3-dependent manner.Molecular biology reports · 2026Article
- Sarcopenic obesity is associated with more severe functional impairment and lumbar degeneration in patients with degenerative lumbar spinal stenosis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Article
- Article
- Smart biophysical cue-based strategies and materials for intervertebral disc degeneration therapy.Bioactive materials · 2026Review
- Integrated Multi-Omics Analysis and Experimental Validation Identify UBE2Q2 as a Candidate Molecule Target in Intervertebral Disc Degeneration.Journal of cellular and molecular medicine · 2026Article
- Antioxidant Nanotherapies for Intervertebral Disk Degeneration: Progress and Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- SETD1A Regulates Glycolysis and Senescence of Nucleus Pulposus Cells via H3K4me3-HELZ2/PPARα-HIF1α Axis to Drive Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Superoxide dismutase in intervertebral disc degeneration: from pathophysiological mechanism to therapeutic strategies.Molecular biology reports · 2026Review
- Efficacy and Mechanisms of Duhuo Jisheng Decoction in Treating Intervertebral Disc Degeneration: A Network Pharmacology and Experimental Study.Current medical science · 2026Article
- Piezo1 in immune cells: from mechanosensation to immunoregulation.Frontiers in immunology · 2026Review
- Resetting the epigenetic clock: cellular senescence and regenerative strategies in intervertebral disc degeneration.Frontiers in aging · 2026Review
- Mechanotransduction in intervertebral disc degeneration: from compartment-specific sensors to translational frontiers.Frontiers in bioengineering and biotechnology · 2026Review
- Plastrum Testudinis Extract Ameliorates Intervertebral Disc Degeneration by Suppressing NF-κB Mediated Senescence and Inflammation.Journal of immunology research · 2026Article
- The Biomechanical Landscape of Lumbar Disc Herniation: Mechanobiological Insights Into Injury and Regeneration.Neurospine · 2026Review
- 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
- Spinal manipulative therapy promotes nucleus pulposus resorption and alleviates pain in a rat model of lumbar disc herniation via JNK-dependent regulation of inflammation and tissue remodeling.American journal of translational research · 2026Article
- Degenerative Disease of Intervertebral Disc: A Narrative Review of Pathogenesis, Clinical Implications and Therapies.Bioengineering (Basel, Switzerland) · 2025Review
- Integrated nanoindentation-Raman spectroscopy reveals microscale biomechanical and molecular biomarkers of early intervertebral disc degeneration in a rat model.Materials today. Bio · 2025Article
- Dual-pathological cascade delivery of apoptotic vesicles for targeted therapy in intervertebral disc degeneration.Materials today. Bio · 2025Article
- Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The senescence of nucleus pulposus cells (NPCs) at the heart of the pathogenesis of intervertebral disc degeneration (IVDD), which causes low back pain. Abnormal mechanical stress causes intracellular Ca Aims: This creates a positive feedback loop of oxidative-inflammatory damage by inducing endoplasmic reticulum stress and mitochondrial reactive oxygen species (ROS) bursts, as well as directly activating the NLRP3 inflammasome/NF-кB axis to promote the release of pro-inflammatory factors like IL-1β. Results: Energy metabolism collapsed as a result of mechanistic cause that caused excessive activation of mitophagy via the ROS-PINK1/Parkin pathway, and SIRT1 functional suppression further compromised mitochondrial quality control. The inflammatory nucleus pulposus (NP) brought on by mechanical stimulation caused macrophages to polarize toward the M1 type, and the p38MAPK pathway was activated by the TNF-α/IL-1β released, which in turn increased senescence markers like p16/p21. Notably, ROS both triggers mitophagy and activates the p53 pathway. On the one hand, oxidative damage-induced ATM/ATR kinase activation leads to p53 phosphorylation, which triggers p21-mediated cell-cycle block. On the other hand, p53 exacerbates mitochondrial dysfunction by inhibiting SIRT1 expression, creating a triangular amplification loop of p53-ROS-mitophagy. Furthermore, p53 stimulates apoptosis by altering the Bax/Bcl-2 balance and works in concert with inflammatory substances secreted by M1-type macrophages to cause the development of senescence-associated secretory phenotype (SASP). Conclusion: This interaction network reveals the dynamic coupling of mechano-immune-metabolic pathways in the course of IVDD, providing a theoretical basis for the development of multi-targeted intervention strategies, such as PIEZO1 inhibitors combined with M2-type macrophage polarization modulation, which are expected to delay disease progression by blocking key nodes.
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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.