ArticleScientific reports2016
Acidic pH promotes intervertebral disc degeneration: Acid-sensing ion channel -3 as a potential therapeutic target.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06169488 (The Lumbar Interbody Fusion vs. Multidisciplinary Rehabilitation), which is not on this map. Cited by 93 papers, 1 of them a synthesis that pooled it.
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.
The Lumbar Interbody Fusion vs. Multidisciplinary Rehabilitation (LIFEHAB) Trial
Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Acid-sensing ion channels mediate the degeneration of intervertebral disc via various pathways-A systematic review.Channels (Austin, Tex.) · 2019Pooled it
- A Portable System for Remote Rehabilitation Following a Total Knee Replacement: A Pilot Randomized Controlled Clinical Study.Sensors (Basel, Switzerland) · 2020Trial
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Causal Effects of Plasma Metabolites on Intervertebral Disc Degeneration and Low Back Pain: A Mendelian Randomization Study.Metabolites · 2026Article
- Surviving the Nucleus Pulposus Desert: Next-Generation Strategies for Intervertebral Disc Cell Therapy.JOR spine · 2026Article
- Spatiotemporal immunomodulation with programmable biomaterials to promote musculoskeletal tissue regeneration.Bioactive materials · 2026Review
- Organ-on-a-Chip Technology: Advances in Modeling Inflammation, Neurovascularization and Nociception in Human Intervertebral Disc Degeneration.Smart medicine · 2026Review
- Preconditioning Mesenchymal Stem Cells to Enhance Performance in the Degenerate Nucleus Pulposus.Tissue engineering. Part B, Reviews · 2026Review
- Defining the Human Nucleus Pulposus Microenvironment and Its Impact on Cell Matrix Synthesis and Metabolic Activity.JOR spine · 2026Article
- Gingerol-loaded hollow manganese dioxide nanoparticles attenuate intervertebral disc oxidative stress.RSC advances · 2026Article
- From Bench to Bedside: Translational Barriers in Mesenchymal Stem Cell Therapy for Intervertebral Disc Degeneration.Bioengineering (Basel, Switzerland) · 2026Review
- Influence of the Intervertebral Disc Microenvironment on Matrix Synthesis and Metabolism in Goat Nucleus Pulposus Cells.JOR spine · 2026Article
- Lactate Metabolism in the Intervertebral Disc: Mechanistic Insights and Pathological Implications.Biomolecules · 2026Review
- Stress-response exhaustion in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2026Review
- Bioactive Therapies for Degenerative Disc Disease: Microenvironmental Foundations of Disease.World neurosurgery · 2025Review
- Electric currents in disc health: The role of ion channels in intervertebral disc pathophysiology.Journal of orthopaedic translation · 2025Review
- Heat shock transcription factor-mediated thermal tolerance and cell size plasticity in marine diatoms.Nature communications · 2025Article
- Parallel Networks to Predict TIMP and Protease Cell Activity of Nucleus Pulposus Cells Exposed and Not Exposed to Pro-Inflammatory Cytokines.JOR spine · 2025Article
- Risk factors and treatment strategies for adjacent segment disease following spinal fusion (Review).Molecular medicine reports · 2025Review
- ASIC1a mediated nucleus pulposus cells pyroptosis and glycolytic crosstalk as a molecular basis for intervertebral disc degeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
The aetiology of intervertebral disc (IVD) degeneration remains poorly understood. Painful IVD degeneration is associated with an acidic intradiscal pH but the response of NP cells to this aberrant microenvironmental factor remains to be fully characterised. The aim here was to address the hypothesis that acidic pH, similar to that found in degenerate IVDs, leads to the altered cell/functional phenotype observed during IVD degeneration, and to investigate the involvement of acid-sensing ion channel (ASIC) -3 in the response. Human NP cells were treated with a range of pH, from that of a non-degenerate (pH 7.4 and 7.1) through to mildly degenerate (pH 6.8) and severely degenerate IVD (pH 6.5 and 6.2). Increasing acidity of pH caused a decrease in cell proliferation and viability, a shift towards matrix catabolism and increased expression of proinflammatory cytokines and pain-related factors. Acidic pH resulted in an increase in ASIC-3 expression. Importantly, inhibition of ASIC-3 prevented the acidic pH induced proinflammatory and pain-related phenotype in NP cells. Acidic pH causes a catabolic and degenerate phenotype in NP cells which is inhibited by blocking ASIC-3 activity, suggesting that this may be a useful therapeutic target for treatment of IVD degeneration.
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