ReviewCellular and molecular life sciences : CMLS2017
Chemokines in neuron-glial cell interaction and pathogenesis of neuropathic pain.
Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 2 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
188 citing papers in PubMed, 2 syntheses or guidelines pooled it, 333 citations in OpenAlex.
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Research trends and hotspots of neuropathic pain in neurodegenerative diseases: a bibliometric analysis.Frontiers in immunology · 2023Pooled it
- Lysophosphatidic acid is associated with neuropathic pain intensity in humans: An exploratory study.PloS one · 2018Trial
- Peripheral Nerve Injury Induces an Interferon-Responsive State Centered on Satellite Glial Cells in the DRG That Sustains Neuropathic Pain Through STAT1 and CXCL10 Signaling.Brain sciences · 2026Article
- Targeting CXCR2 in Nociceptive Sensory Neurons Offers Novel Therapeutic Potentials for Postoperative Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuromodulation Techniques Alleviating Neuropathic Pain by Targeting Microglia: A Narrative Review.Pain and therapy · 2026Review
- TGF-β1 inhibits CXCL1/CXCR2 signaling pathway to alleviate neuropathic pain in a spinal nerve ligation rat model.Journal of molecular histology · 2026Article
- Lidocaine alleviates diabetic neuropathic pain by inhibiting spinal astrocyte activation through modulation of the CXCL13/CXCR5 axis.Journal of molecular histology · 2026Article
- The effect of tumor necrosis factor-alpha on rheumatoid arthritis-related pain: overview of evidence and mechanistic pathways.Croatian medical journal · 2026Review
- Spared Nerve Injury Induces Long-Term and Brain Region-Specific Changes in Oligodendrocyte Density in Mice.European journal of pain (London, England) · 2026Article
- Clinical characteristics of autoimmune glial fibrillary acidic protein astrocytopathy in adults: a retrospective analysis of 9 cases.Internal medicine journal · 2026Article
- Repetitive transcranial magnetic stimulation modulates neuroinflammation and cell apoptosis via the interaction between Ifit3 and Stat1 for the treatment of neuropathic pain.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Contribution of proneurotrophin-3 to nerve trauma-induced neuropathic pain through promoting TrkC-mediated increase of CCL2 in primary sensory neurons.Brain, behavior, and immunity · 2026Article
- Study on the Analgesic Mechanism of Aloperine in Mice with Neuropathic Pain Based on the p38MAPK/FKN/CX3CR1 Pathway.Molecular neurobiology · 2026Article
- Cognitive Behavioral Therapy and Pain Chronification: Neuroimmune Rationale, Evidence Boundaries, and Trial Design Priorities: A Structured Narrative Review.Journal of pain research · 2026Review
- Association of Inflammatory Proteins with Neuropathic Pain: A Two-Sample Bidirectional Mendelian Randomization.Journal of pain research · 2026Article
- Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain.Journal of pain research · 2026Review
- Review
- The function of chemokine-driven glial-neuronal interaction in chronic pain.Frontiers in neuroscience · 2026Review
- Neuroimmune Crosstalk in Psoriasis: Mechanisms and Therapeutic Implications.Inflammation · 2025Review
128 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain resulting from damage or dysfunction of the nervous system is a highly debilitating chronic pain state and is often resistant to currently available treatments. It has become clear that neuroinflammation, mainly mediated by proinflammatory cytokines and chemokines, plays an important role in the establishment and maintenance of neuropathic pain. Chemokines were originally identified as regulators of peripheral immune cell trafficking and were also expressed in neurons and glial cells in the central nervous system. In recent years, accumulating studies have revealed the expression, distribution and function of chemokines in the spinal cord under chronic pain conditions. In this review, we provide evidence showing that several chemokines are upregulated after peripheral nerve injury and contribute to the pathogenesis of neuropathic pain via different forms of neuron-glia interaction in the spinal cord. First, chemokine CX3CL1 is expressed in primary afferents and spinal neurons and induces microglial activation via its microglial receptor CX3CR1 (neuron-to-microglia signaling). Second, CCL2 and CXCL1 are expressed in spinal astrocytes and act on CCR2 and CXCR2 in spinal neurons to increase excitatory synaptic transmission (astrocyte-to-neuron signaling). Third, we recently identified that CXCL13 is highly upregulated in spinal neurons after spinal nerve ligation and induces spinal astrocyte activation via receptor CXCR5 (neuron-to-astrocyte signaling). Strategies that target chemokine-mediated neuron-glia interactions may lead to novel therapies for the treatment of neuropathic pain.
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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.