ArticleJournal of neuroinflammation2018
miRNA-23a/CXCR4 regulates neuropathic pain via directly targeting TXNIP/NLRP3 inflammasome axis.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 184 citations in OpenAlex.
- Mapping the research landscape of microRNAs in pain: a comprehensive bibliometric analysis.Frontiers in molecular neuroscience · 2024Pooled it
- The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review.Journal of clinical laboratory analysis · 2022Pooled it
- Neuropathic Pain: Mapping the miRNA Landscape.Non-coding RNA · 2026Review
- Investigation of miRNAs Associated with Inflammation and Apoptosis in Patients with Idiopathic Trigeminal Neuralgia.Diagnostics (Basel, Switzerland) · 2026Article
- Alteration of microRNA Expression Associated with Chronic Back Pain in Patients with Intervertebral Disc Degeneration: A Scoping Review.International journal of molecular sciences · 2026Article
- New insight into RNA biomarkers in neuropathic pain: a clinician-neuroscientist roadmap to translational testing and treatment monitoring a clinical review.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Plasma-derived exosomal miR-144-3p targeting IL-1β is involved in pressure pain threshold regulation at PC6 acupoint in myocardial ischemia rats.Journal of traditional and complementary medicine · 2026Article
- PD-1 Attenuates Neuropathic Pain by Ameliorating NLRP3 Inflammasome-Mediated Microglia Pyroptosis.Molecular neurobiology · 2025Article
- Roles of noncoding RNAs in neuropathic pain.Pain reports · 2025Review
- NLRP3 inflammasome: a key driver of neuroinflammation and a novel therapeutic target for neuropathic pain.Anesthesia and pain medicine · 2025Review
- MicroRNA-Based Delivery Systems for Chronic Neuropathic Pain Treatment in Dorsal Root Ganglion.Pharmaceutics · 2025Review
- WERF Endometriosis Phenome and Biobanking Harmonisation Project for Experimental Models in Endometriosis Research (EPHect-EM-Pain): methods to assess pain behaviour in rodent models of endometriosis.Molecular human reproduction · 2025Review
- The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.Aging and disease · 2025Review
- Unveiling the Mechanisms of Pain in Endometriosis: Comprehensive Analysis of Inflammatory Sensitization and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Immunomodulation with M2 macrophage-derived extracellular vesicles for enhanced titanium implant osseointegration under diabetic conditions.Materials today. Bio · 2025Article
- Gynostemma pentaphyllum (Thunb.) Makino Affects Autophagy and Improves Diabetic Peripheral Neuropathy Through TXNIP-Mediated PI3K/AKT/mTOR Signaling Pathway.Applied biochemistry and biotechnology · 2025Article
- Biosynthesis inhibition of miR-142-5p in a NCellular & molecular biology letters · 2025Article
- Macrophage to neuron communication via extracellular vesicles in neuropathic pain conditions.Heliyon · 2025Article
- Exosome-mediated miRNA delivery: a molecular switch for reshaping neuropathic pain therapy.Frontiers in molecular neuroscience · 2025Review
- The CXCL12/CXCR4 Axis: An Emerging Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
51 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
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundChemokine CXC receptor 4 (CXCR4) in spinal glial cells has been implicated in neuropathic pain. However, the regulatory cascades of CXCR4 in neuropathic pain remain elusive. Here, we investigated the functional regulatory role of miRNAs in the pain process and its interplay with CXCR4 and its downstream signaling.
methodsmiRNAs and CXCR4 and its downstream signaling molecules were measured in the spinal cords of mice with sciatic nerve injury via partial sciatic nerve ligation (pSNL). Immunoblotting, immunofluorescence, immunoprecipitation, and mammal two-hybrid and behavioral tests were used to explore the downstream CXCR4-dependent signaling pathway.
resultsCXCR4 expression increased in spinal glial cells of mice with pSNL-induced neuropathic pain. Blocking CXCR4 alleviated the pain behavior; contrarily, overexpressing CXCR4 induced pain hypersensitivity. MicroRNA-23a-3p (miR-23a) directly bounds to 3' UTR of CXCR4 mRNA. pSNL-induced neuropathic pain significantly reduced mRNA expression of miR-23a. Overexpression of miR-23a by intrathecal injection of miR-23a mimics or lentivirus reduced spinal CXCR4 and prevented pSNL-induced neuropathic pain. In contrast, knockdown of miR-23a by intrathecal injection of miR-23a inhibitor or lentivirus induced pain-like behavior, which was reduced by CXCR4 inhibition. Additionally, miR-23a knockdown or CXCR4 overexpression in naïve mice could increase the thioredoxin-interacting protein (TXNIP), which was associated with induction of NOD-like receptor protein 3 (NLRP3) inflammasome. Indeed, CXCR4 and TXNIP were co-expressed. The mammal two-hybrid assay revealed the direct interaction between CXCR4 and TXNIP, which was increased in the spinal cord of pSNL mice. In particular, inhibition of TXNIP reversed pain behavior elicited by pSNL, miR-23a knockdown, or CXCR4 overexpression. Moreover, miR-23a overexpression or CXCR4 knockdown inhibited the increase of TXNIP and NLRP3 inflammasome in pSNL mice.
conclusionsmiR-23a, by directly targeting CXCR4, regulates neuropathic pain via TXNIP/NLRP3 inflammasome axis in spinal glial cells. Epigenetic interventions against miR-23a, CXCR4, or TXNIP may potentially serve as novel therapeutic avenues in treating peripheral nerve injury-induced nociceptive hypersensitivity.
Indexed as
Identifiers
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.