ArticleJournal of neuroinflammation2021
Red nucleus IL-33 facilitates the early development of mononeuropathic pain in male rats by inducing TNF-α through activating ERK, p38 MAPK, and JAK2/STAT3.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis 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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- The role of IL-33 in depression: a systematic review and meta-analysis.Frontiers in psychiatry · 2023Pooled it
- A Novel Long-range Excitatory Neural Circuit from the Magnocellular Red Nucleus to Spinal Dorsal Horn Facilitates Neuropathic Pain-like Behaviors in Male Mice.Neuroscience bulletin · 2026Article
- Targeting Microglia-Neuron Crosstalk to Regulate Neuronal Excitability: Novel Translational Approaches for Chronic Pain Intervention.International journal of molecular sciences · 2026Review
- ZFP612 controls neuropathic pain through epigenetic repression of Il1rl1 within the silencer-promoter loop in primary sensory neurons of male mice.Nature communications · 2025Article
- Ganoderma lucidum polysaccharide attenuates retinal ischemia-reperfusion injury by regulating microglial M1/M2 polarization, suppressing neuroinflammation and inhibiting JAK2/STAT3 pathway.Biochemistry and biophysics reports · 2025Article
- Single-cell transcriptomics identify a novel macrophage population associated with bone invasion in pituitary neuroendocrine tumors.Journal of experimental & clinical cancer research : CR · 2025Article
- Exploring the potential of a thermosensitiveFrontiers in pharmacology · 2025Article
- Environmental enrichment for neuropathic pain via modulation of neuroinflammation.Frontiers in molecular neuroscience · 2025Review
- Navigating the Neuroimmunomodulation Frontier: Pioneering Approaches and Promising Horizons-A Comprehensive Review.International journal of molecular sciences · 2024Review
- Prokineticin-2 Participates in Chronic Constriction Injury-Triggered Neuropathic Pain and Anxiety via Regulated by NF-κB in Nucleus Accumbens Shell in Rats.Molecular neurobiology · 2024Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat model.Neural regeneration research · 2024Article
- Targeting the JAK2/STAT3 signaling pathway for chronic pain.Aging and disease · 2024Review
- Effects of carbamazepine on BDNF expression in trigeminal ganglia and serum in rats with trigeminal neuralgia.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- SHED-derived exosomes attenuate trigeminal neuralgia after CCI of the infraorbital nerve in mice via the miR-24-3p/IL-1R1/p-p38 MAPK pathway.Journal of nanobiotechnology · 2023Article
- ATP/IL-33-Co-Sensing by Mast Cells (MCs) Requires Activated c-Kit to Ensure Effective Cytokine Responses.Cells · 2023Article
- Glycyrrhizic Acid Protects Glomerular Podocytes Induced by High Glucose by Modulating SNARK/AMPK Signaling Pathway.Current medical science · 2023Article
- An Overview of the Mechanisms Involved in Neuralgia.Journal of inflammation research · 2023Review
- Distinct neural networks derived from galanin-containing nociceptors and neurotensin-expressing pruriceptors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Positive interaction between GPER and β-alanine in the dorsal root ganglion uncovers potential mechanisms: mediating continuous neuronal sensitization and neuroinflammation responses in neuropathic pain.Journal of neuroinflammation · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundOur recent studies have identified that the red nucleus (RN) dual-directionally modulates the development and maintenance of mononeuropathic pain through secreting proinflammatory and anti-inflammatory cytokines. Here, we further explored the action of red nucleus IL-33 in the early development of mononeuropathic pain.
methodsIn this study, male rats with spared nerve injury (SNI) were used as mononeuropathic pain model. Immunohistochemistry, Western blotting, and behavioral testing were used to assess the expressions, cellular distributions, and actions of red nucleus IL-33 and its related downstream signaling molecules.
resultsIL-33 and its receptor ST2 were constitutively expressed in the RN in naive rats. After SNI, both IL-33 and ST2 were upregulated significantly at 3 days and peaked at 1 week post-injury, especially in RN neurons, oligodendrocytes, and microglia. Blockade of red nucleus IL-33 with anti-IL-33 neutralizing antibody attenuated SNI-induced mononeuropathic pain, while intrarubral administration of exogenous IL-33 evoked mechanical hypersensitivity in naive rats. Red nucleus IL-33 generated an algesic effect in the early development of SNI-induced mononeuropathic pain through activating NF-κB, ERK, p38 MAPK, and JAK2/STAT3, suppression of NF-κB, ERK, p38 MAPK, and JAK2/STAT3 with corresponding inhibitors markedly attenuated SNI-induced mononeuropathic pain or IL-33-evoked mechanical hypersensitivity in naive rats. Red nucleus IL-33 contributed to SNI-induced mononeuropathic pain by stimulating TNF-α expression, which could be abolished by administration of inhibitors against ERK, p38 MAPK, and JAK2/STAT3, but not NF-κB.
conclusionsThese results suggest that red nucleus IL-33 facilitates the early development of mononeuropathic pain through activating NF-κB, ERK, p38 MAPK, and JAK2/STAT3. IL-33 mediates algesic effect partly by inducing TNF-α through activating ERK, p38 MAPK and JAK2/STAT3.
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.