ArticleJournal of neuroinflammation2021
Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis.
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 30 papers.
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Who cites it
30 citing papers in PubMed, 59 citations in OpenAlex.
- Sex differences in TLR4 expression in SHR do not contribute to sex differences in blood pressure or the renal T cell profile.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Trial
- Spinal neuronal TLR4-induced enhancement of nociceptive signals contributes to myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- The Effects and Mechanisms Underlying Red Meat Diet on Endometriosis Through Modulating Gut Microbiota.Food science & nutrition · 2026Article
- Somatic Cancer Driver Mutation Analysis in Endometriosis with Tumor-like Presentations: A Case Series Study.Biomedicines · 2026Article
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- The AGE-RAGE Pathway in Endometriosis: A Focused Mechanistic Review and Structured Evidence Map.International journal of molecular sciences · 2026Review
- The microbiome-inflammasome axis in endometriosis-associated chronic pelvic pain: mechanisms and therapeutic opportunities from an immunological perspective.Frontiers in immunology · 2026Review
- Tetramethylpyrazine Confers Protection Against Oxidative Stress and NLRP3-Dependent Pyroptosis in Rats with Endometriosis.Organogenesis · 2025Article
- Article
- Bromodomain-containing protein 4 contributes to chronic postsurgical pain via activating TLR4/NF-kappaB-dependent neuroinflammation.BMC anesthesiology · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- [Mechanisms of Neiyiting Decoction in Preventing Postoperative Recurrence of Endometriosis by Inhibiting Macrophage M1 Polarization Through the TREM1/TLR4/NF-κB Signaling Pathway].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Article
- Unveiling the Mechanisms of Pain in Endometriosis: Comprehensive Analysis of Inflammatory Sensitization and Therapeutic Potential.International journal of molecular sciences · 2025Review
- TLR4 Targeting: A Promising Therapeutic Approach Across Multiple Human Diseases.Current protein & peptide science · 2025Review
- Myeloid Differentiation Primary Response Protein 88: An Important Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
- SARS-CoV-2 viral proteins trigger pain via TLR2/4-MyD88 pathway.Frontiers in molecular neuroscience · 2025Article
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- IL-6 from cerebrospinal fluid causes widespread pain via STAT3-mediated astrocytosis in chronic constriction injury of the infraorbital nerve.Journal of neuroinflammation · 2024Article
- Artemvulactone E isolated fromFrontiers in pharmacology · 2024Article
- Recent advances in the treatment of pain in endometriosis: A bibliometric analysis of experimental models.Veterinary world · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAs a classic innate immunity pathway, Toll-like receptor 4 (TLR4) signaling has been intensively investigated for its function of pathogen recognition. The receptor is located not only on immune cells but also on sensory neurons and spinal glia. Recent studies revealed the involvement of neuronal TLR4 in different types of pain. However, the specific role of TLR4 signaling in the pain symptom of endometriosis (EM) remains obscure.
methodsThe rat endometriosis model was established by transplanting uterine horn tissue into gastrocnemius. Western blotting and/or immunofluorescent staining were applied to detect high mobility group box 1 (HMGB1), TLR4, myeloid differentiation factor-88 adaptor protein (MyD88), and nuclear factor kappa-B-p65 (NF-κB-p65) expression, as well as the activation of astrocyte and microglia. The antagonist of TLR4 (LPS-RS-Ultra, LRU) and MyD88 homodimerization inhibitory peptide (MIP) were intrathecally administrated to assess the behavioral effects of blocking TLR4 signaling on endometriosis-related pain.
resultsMechanical hyperalgesia was observed at the graft site, while HMGB1 was upregulated in the implanted uterine tissue, dorsal root ganglion (DRG), and spinal dorsal horn (SDH). Compared with sham group, upregulated TLR4, MyD88, and phosphorylated NF-κB-p65 were detected in the DRG and SDH in EM rats. The activation of astrocytes and microglia in the SDH was also confirmed in EM rats. Intrathecal application of LRU and MIP alleviated mechanical pain on the graft site of EM rats, with decreased phosphorylation of NF-κB-p65 in the DRG and reduced activation of glia in the SDH.
conclusionsHMGB1-TLR4-MyD88 signaling pathway in the DRG and SDH may involve in endometriosis-related hyperpathia. Blockade of TLR4 and MyD88 might serve as a potential treatment for pain in endometriosis.
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