ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
NFAT1 Orchestrates Spinal Microglial Transcription and Promotes Microglial Proliferation via c-MYC Contributing to Nerve Injury-Induced Neuropathic Pain.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Peripheral and central changes induced by neural mobilization in animal models of neuropathic pain: a systematic review.Frontiers in neurology · 2023Pooled it
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Calcineurin/NFAT signaling in the temporal integration of Ca²⁺ stress in neurodegeneration.Cell death discovery · 2026Review
- Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury-induced neuropathic pain.Neural regeneration research · 2026Article
- Targeting CIRP and IL-6R-mediated microglial inflammation to improve outcomes in intracerebral hemorrhage.Journal of advanced research · 2026Article
- PRMT6 inhibition or deficiency attenuates diabetic neuropathic pain in male mice and is associated with reduced spinal neuroinflammation, microgliosis, and altered p53-p21 signaling.Journal of neuroinflammation · 2026Article
- Spinal Cord Stimulation Alleviates Neuropathic Pain Involves Regulation of the CaCellular and molecular neurobiology · 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
- NFAT1Cellular & molecular biology letters · 2026Article
- TET2 in epigenetic control of immune cells: Implications for inflammatory responses and age-related pathologies.The Journal of biological chemistry · 2026Review
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- Immunosuppressant treatment reduces cocaine-induced behavioral sensitization in mice.Frontiers in pharmacology · 2026Article
- Multi-Omics Analysis Reveals Nono-Kcnq2 Regulation of Neuronal Excitability in Chronic Constriction Injury-Induced Neuropathic Pain.Research (Washington, D.C.) · 2026Article
- Demyelination-related pain: role of lysophosphatidic acid in satellite glial cell-neuron crosstalk.Journal of translational medicine · 2025Article
- GDF11 Mitigates Neuropathic Pain via Regulation of Microglial Polarization and Neuroinflammation through TGF-βR1/SMAD2/NF-κB Pathway in Male Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- NFAT1 Signaling Contributes to Bone Cancer Pain by Regulating IL-18 Expression in Spinal Microglia.CNS neuroscience & therapeutics · 2025Article
- Neuraminidase 1 regulates neuropathogenesis by governing the cellular state of microglia via modulation of Trem2 sialylation.Cell reports · 2025Article
- An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord.Communications biology · 2025Article
- Effective protection of biological tissues from severe blunt force injury by engineered nanoscale liquid flow.Scientific reports · 2024Article
- Single cell analysis reveals the roles and regulatory mechanisms of type-I interferons in Parkinson's disease.Cell communication and signaling : CCS · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Peripheral nerve injury-induced spinal microglial proliferation plays a pivotal role in neuropathic pain. So far, key intracellular druggable molecules involved in this process are not identified. The nuclear factor of activated T-cells (NFAT1) is a master regulator of immune cell proliferation. Whether and how NFAT1 modulates spinal microglial proliferation during neuropathic pain remain unknown. Here it is reported that NFAT1 is persistently upregulated in microglia after spinal nerve ligation (SNL), which is regulated by TET2-mediated DNA demethylation. Global or microglia-specific deletion of Nfat1 attenuates SNL-induced pain and decreases excitatory synaptic transmission of lamina II neurons. Furthermore, deletion of Nfat1 decreases microglial proliferation and the expression of multiple microglia-related genes, such as cytokines, transmembrane signaling receptors, and transcription factors. Particularly, SNL increases the binding of NFAT1 with the promoter of Itgam, Tnf, Il-1b, and c-Myc in the spinal cord. Microglia-specific overexpression of c-MYC induces pain hypersensitivity and microglial proliferation. Finally, inhibiting NFAT1 and c-MYC by intrathecal injection of inhibitor or siRNA alleviates SNL-induced neuropathic pain. Collectively, NFAT1 is a hub transcription factor that regulates microglial proliferation via c-MYC and guides the expression of the activated microglia genome. Thus, NFAT1 may be an effective target for treating neuropathic pain.
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What Socratic 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 Socratic graph.