ArticleThe Journal of clinical investigation2024
METTL14-mediated m6A epitranscriptomic modification contributes to chemotherapy-induced neuropathic pain by stabilizing GluN2A expression via IGF2BP2.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- CircRHBDD1(4,5) drives malignant progression of oral squamous cell carcinoma by enhancing DKK1 mRNA stability through facilitating mOncogene · 2026Article
- METTL3-mediated m6A modification of circMtmr7 contributes to paclitaxel-induced peripheral neuropathy in the dorsal horn.The Journal of physiology · 2026Article
- mNature reviews. Neuroscience · 2026Review
- Complement-inflammation inhibition via stealth nanomedicine for mild thermo-responsive postoperative on-demand pain management.Materials today. Bio · 2026Article
- GWAS of extended prescription analgesic use identifies genetic loci in chronic pain.Nature communications · 2026Article
- Review
- Histone Lactylation Contributes to Neuropathic Pain by Facilitating mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Article
- 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
- CAPRIN1 specifically mediates mCommunications biology · 2025Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- Shentong Zhuyu Decoction Alleviates Neuropathic Pain in Mice by Inhibiting the NMDAR-2B Receptor-Mediated CaMKII/CREB Signaling Pathway in GABAergic Neurons of the Interpeduncular Nucleus.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Spi1 aggravates neuropathic pain by modulating Clec7a-mediated neuroinflammation and microglial phagocytosis.The journal of headache and pain · 2025Article
- Pia Mater-Penetrable Lipopolymer Nanoparticles for Gliocyte-Targeted IL-10 mRNA Therapy Alleviate Paclitaxel-Induced Peripheral Neuropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An Investigation of the RNA Modification mInternational journal of molecular sciences · 2025Article
- Article
- IMPlications of IMP2 in RNA Biology and Disease.International journal of molecular sciences · 2025Review
- Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review).Molecular medicine reports · 2025Review
- Unraveling the landscape of m6A RNA methylation in wound healing and scars.Cell death discovery · 2024Review
- FTO-mediated DSP mMolecular cancer · 2024Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetics is a biological process that modifies and regulates gene expression, affects neuronal function, and contributes to pain. However, the mechanism by which epigenetics facilitates and maintains chronic pain is poorly understood. We aimed to determine whether N6-methyladenosine (m6A) specifically modified by methyltransferase-like 14 (METTL14) alters neuronal activity and governs pain by sensitizing the GluN2A subunit of the N-methyl-d-aspartate receptor (NMDAR) in the dorsal root ganglion (DRG) neurons in a model of chemotherapy-induced neuropathic pain (CINP). Using dot blotting, immunofluorescence, gain/loss-of-function, and behavioral assays, we found that m6A levels were upregulated in L4-L6 DRG neurons in CINP in a DBP/METTL14-dependent manner, which was also confirmed in human DRGs. Blocking METTL14 reduced m6A methylation and attenuated pain hypersensitivity. Mechanistically, METTL14-mediated m6A modification facilitated the synaptic plasticity of DRG neurons by enhancing the GluN2A subunit of NMDAR, and inhibiting METTL14 blocked this effect. In contrast, overexpression of METTL14 upregulated m6A modifications, enhanced presynaptic NMDAR activity in DRG neurons, and facilitated pain sensation. Our findings reveal a previously unrecognized mechanism of METTL14-mediated m6A modification in DRG neurons to maintain neuropathic pain. Targeting these molecules may provide a new strategy for pain treatment.
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