ArticlePain2021
Methyltransferase-like 3 contributes to inflammatory pain by targeting TET1 in YTHDF2-dependent manner.
Article in Pain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 51 citations in OpenAlex.
- Exercise, Demethylase FTO, Neurological Disorders, and Neuropathic Pain: Potential Molecular Mechanisms.CNS neuroscience & therapeutics · 2026Review
- Inhibition of YTHDF2-mediated CYLD mRNA degradation promotes neuronal ferroptosis and pain in Parkinson's disease through NOX4 deubiquitination.Cell biology and toxicology · 2026Article
- Spinal Cord CELF4 in Chronic Constriction Injury-Induced Neuropathic Pain: Association with TRPV1 and COX-2 Expression.Journal of molecular neuroscience : MN · 2026Article
- Review
- Manipulation therapy alleviates neuropathic painThe Korean journal of pain · 2026Article
- Acute and chronic stress differentially regulate pain via distinct ensembles in the paraventricular nucleus of hypothalamus.Molecular psychiatry · 2026Article
- 5-HT2C receptors in the glutamatergic neurons of dorsal raphe nucleus orchestrate the comorbidity of pain and anxiety in mice.BMC medicine · 2026Article
- Histone Lactylation Contributes to Neuropathic Pain by Facilitating mThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Dorsal Root Ganglion as a Hub for Peripheral Sensitization: A Hierarchical Regulation Model and Translational Progress.Journal of pain research · 2026Review
- METTL4 regulates synaptic UCP2 N6-adenosine methylation to mediate pain hypersensitivity in female mice.Cellular and molecular life sciences : CMLS · 2025Article
- Gut microbes-spinal connection is required for itch sensation.Gut microbes · 2025Article
- SERBP1-PCIF1 complex-controlled m6Am modification in glutamatergic neurons of the primary somatosensory cortex is required for neuropathic pain in mice.Nature communications · 2025Article
- Transcriptomic analysis of the m6A reader YTHDF2 in the maintenance and differentiation of human embryonic stem cells.Stem cells (Dayton, Ohio) · 2025Article
- NAT10 inhibition alleviates astrocyte autophagy by impeding ac4C acetylation ofActa pharmaceutica Sinica. B · 2025Article
- Kv3.1 Interaction with UBR5 Is Required for Chronic Inflammatory Pain.Molecular neurobiology · 2025Article
- TET1 Participates in Complete Freund's Adjuvant-induced Trigeminal Inflammatory Pain by Regulating Kv7.2 in a Mouse Model.Neuroscience bulletin · 2024Article
- Article
- FOXD3-mediated transactivation of ALKBH5 promotes neuropathic pain via mProceedings of the National Academy of Sciences of the United States of America · 2024Article
- METTL14-mediated m6A epitranscriptomic modification contributes to chemotherapy-induced neuropathic pain by stabilizing GluN2A expression via IGF2BP2.The Journal of clinical investigation · 2024Article
- Spinal-Specific Super Enhancer in Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractThe methyltransferase-like 3 (Mettl3) is a key component of the large N6-adenosine-methyltransferase complex in mammalian responsible for RNA N6-methyladenosine (m6A) modification, which plays an important role in gene post-transcription modulation. Although RNA m6A is enriched in mammalian neurons, its regulatory function in nociceptive information processing remains elusive. Here, we reported that Complete Freund's Adjuvant (CFA)-induced inflammatory pain significantly decreased global m6A level and m6A writer Mettl3 in the spinal cord. Mimicking this decease by knocking down or conditionally deleting spinal Mettl3 elevated the levels of m6A in ten-eleven translocation methylcytosine dioxygenases 1 (Tet1) mRNA and TET1 protein in the spinal cord, leading to production of pain hypersensitivity. By contrast, overexpressing Mettl3 reversed a loss of m6A in Tet1 mRNA and blocked the CFA-induced increase of TET1 in the spinal cord, resulting in the attenuation of pain behavior. Furthermore, the decreased level of spinal YT521-B homology domain family protein 2 (YTHDF2), an RNA m6A reader, stabilized upregulation of spinal TET1 because of the reduction of Tet1 mRNA decay by the binding to m6A in Tet1 mRNA in the spinal cord after CFA. This study reveals a novel mechanism for downregulated spinal cord METTL3 coordinating with YTHDF2 contributes to the modulation of inflammatory pain through stabilizing upregulation of TET1 in spinal neurons.
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