ArticleJournal of neuroinflammation2017
Suppression of MyD88-dependent signaling alleviates neuropathic pain induced by peripheral nerve injury in the rat.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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
40 citing papers in PubMed, 82 citations in OpenAlex.
- Presurgical immune biomarkers associated with pain intensity and pain interference recovery after total knee arthroplasty: findings from the PRIME-KNEE study.medRxiv : the preprint server for health sciences · 2026Article
- Selenoprotein P deletion ameliorates metabolic stress-associated anxiety-like behavior in male mice.Endocrinology · 2026Article
- MiR-298 suppresses astrocytic NF-κB activity and neuroinflammationThe Korean journal of pain · 2025Article
- ( +)-Catechin Alleviates CCI-Induced Neuropathic Pain by Modulating Microglia M1 and M2 Polarization via the TLR4/MyD88/NF-κB Signaling Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Low intensity trans-spinal focused ultrasound reduces mechanical sensitivity and suppresses spinal microglia activation in rats with chronic constriction injury.Bioelectronic medicine · 2025Article
- Myeloid Differentiation Primary Response Protein 88: An Important Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
- Low-Dose IL-2 Attenuates Neuropathic Pain via Treg Expansion in Rats.Journal of pain research · 2025Article
- Exosomal GDNF from Bone Marrow Mesenchymal Stem Cells Moderates Neuropathic Pain in a Rat Model of Chronic Constriction Injury.Neuromolecular medicine · 2024Article
- Neuronal C-Reactive Protein/FcγRI Positive Feedback Proinflammatory Signaling Contributes to Nerve Injury Induced Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- CircUBE3B High Expression Participates in Sevoflurane-Induced Human Hippocampal Neuron Injury via Targeting miR-326 and Regulating MYD88 Expression.Neurotoxicity research · 2023Article
- Chronic constriction injury-induced changes in circular RNA expression profiling of the dorsal root ganglion in a rat model of neuropathic pain.BMC neuroscience · 2022Article
- Regulation of Neuroinflammatory Signaling by PPARγ Agonist in Mouse Model of Diabetes.International journal of molecular sciences · 2022Article
- Resveratrol Ameliorates Trigeminal Neuralgia-Induced Cognitive Deficits by Regulating Neural Ultrastructural Remodelling and the CREB/BDNF Pathway in Rats.Oxidative medicine and cellular longevity · 2022Article
- Protective role of ethyl pyruvate in spinal cord injury by inhibiting the high mobility group box-1/toll-like receptor4/nuclear factor-kappa B signaling pathway.Frontiers in molecular neuroscience · 2022Review
- Neuronal toll like receptor 9 contributes to complete Freund's adjuvant-induced inflammatory pain in mice.Frontiers in molecular neuroscience · 2022Article
- Combination of autophagy and NFE2L2/NRF2 activation as a treatment approach for neuropathic pain.Autophagy · 2021Article
- The citrullinated/native index of autoantibodies against hnRNP-DL predicts an individual "window of treatment success" in RA patients.Arthritis research & therapy · 2021Article
- Lidocaine Alleviates Neuropathic Pain and Neuroinflammation by Inhibiting HMGB1 Expression to Mediate MIP-1α/CCR1 Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Effects of CMYA1 overexpression on cardiac structure and function in mice.Acta biochimica et biophysica Sinica · 2021Article
- Therapeutic effects of peripherally administrated neural crest stem cells on pain and spinal cord changes after sciatic nerve transection.Stem cell research & therapy · 2021Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyD88 is the adaptor protein of MyD88-dependent signaling pathway of TLRs and IL-1 receptor and regulates innate immune response. However, it was not clear whether and how MyD88 and related signaling pathways in the dorsal root ganglion (DRG) and spinal dorsal horn (SDH) are involved in neuropathic pain.
methodsChronic constriction injury (CCI) was used to induce neuropathic pain in the rat. The expression of MyD88, TRIF, IBA1, and GFAP was detected with immunofluorescent staining and Western blot. The expression of interleukin-1 beta (IL-1β), high mobility group box 1 (HMGB1), NF-κB-p65, phosphorylated NF-κB-p65, ERK, phosphorylated ERK, and tumor necrosis factor-alpha (TNF-α) was detected with Western blot. Pain-related behavioral effects of MyD88 homodimerization inhibitory peptide (MIP) were accessed up to 3 weeks after intrathecal administration.
resultsPeripheral nerve injury significantly increased the protein level of MyD88 in the DRG and SDH, but had no effect on TRIF. MyD88 was found partly distributed in the nociceptive neurons in the DRGs and the astrocytes and microglia in the SDH. HMGB1 and IL-1β were also found upregulated in nociceptive pathways of CCI rats. Intrathecal application of MIP significantly alleviated mechanical and thermal hyperalgesia in the CCI rats and also reversed CCI-induced upregulation of MyD88 in both DRG and SDH. Further investigation revealed that suppression of MyD88 protein reduced the release of TNF-α and glial activation in the SDH in the CCI rats.
conclusionsMyD88-dependent TIR pathway in the DRG and SDH may play a role in CCI-induced neuropathic pain. MyD88 might serve as a potential therapeutic target for neuropathic pain.
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.