ArticleCell & bioscience2020
Botulinum toxin type A alleviates neuropathic pain and suppresses inflammatory cytokines release from microglia by targeting TLR2/MyD88 and SNAP23.
Article in Cell & bioscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Dose-Dependent Effects of Botulinum Toxin Type A on Prevention of Postoperative Scars in Various Regions in the Body: A Prospective, Double-Blind Randomized Controlled Trial.Aesthetic plastic surgery · 2025Trial
- Untangling neuropathic pain: pathophysiological insights and future directions for targeted therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Botulinum toxin type A inhibits chronic post-thoracotomy pain through the HMGB1-mediated TLR4/NF-κB signaling pathway.American journal of translational research · 2026Article
- Targeting macrophage function with botulinum toxin: a novel translational strategy for preventing and treating pathological scars.Postepy dermatologii i alergologii · 2026Review
- Botulinum Toxin Type A Reduces Pain and NF-κB Levels in a Rat Model of Complex Regional Pain Syndrome.Journal of pain research · 2026Article
- Identification of Neurotrophic Factor Related Biomarkers and Mechanistic Insights into Neuropathic Pain via Integrated Bioinformatics Analysis.ACS omega · 2025Article
- Botulinum toxin type A inhibits microglia pyroptosis by suppressing Cblb-mediated degradation of Pdlim1 to attenuate neuropathic pain.The journal of headache and pain · 2025Article
- Activation of NR2A-Wnt-TLR2 Signaling Axis in Satellite Glial Cells of the Dorsal Root Ganglion Contributes to Neuropathic Pain Induced by Nerve Injury in Diabetic Mice.Molecular neurobiology · 2025Article
- Pioneering pain management with botulinum toxin type A: From anti-inflammation to regenerative therapies.Heliyon · 2025Review
- Utility of blood DNA methylation and immune cell-type estimates to identify clinically relevant links between immunity and health conditions in a large cohort.Frontiers in immunology · 2025Article
- Myeloid Differentiation Primary Response Protein 88: An Important Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
- Neurobiological mechanisms of botulinum neurotoxin-induced analgesia for neuropathic pain.Pharmacology & therapeutics · 2024Review
- TLR2 Mediates Microglial Activation and Contributes to Central Sensitization in a Recurrent Nitroglycerin-induced Chronic Migraine Model.Molecular neurobiology · 2024Article
- Single-cell RNA sequencing reveals roles of unique retinal microglia types in early diabetic retinopathy.Diabetology & metabolic syndrome · 2024Article
- rTMS and TENS Relieve Neuropathic Pain in CCI Model Rats by Modulating Central Nervous System TRPV1 and Neuroinflammation.Mediators of inflammation · 2024Article
- Toll-like Receptor 2-Melatonin Feedback Loop Regulates the Activation of Spinal NLRP3 Inflammasome in Morphine-Tolerant Rats.Neurochemical research · 2023Article
- Effect of botulinum toxin type A on non-motor symptoms and quality of life in Meige syndrome.Frontiers in neurology · 2023Article
- The Roles of Imaging Biomarkers in the Management of Chronic Neuropathic Pain.International journal of molecular sciences · 2022Review
- Review
- Dramatic Effect of Botulinum Toxin Type A on Hypertrophic Scar: A Promising Therapeutic Drug and Its Mechanism Through the SP-NK1R Pathway in Cutaneous Neurogenic Inflammation.Frontiers in medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundBotulinum toxin type A (BTX-A) was considered to be a new potential drug for neuropathic pain (NP) treatment.
resultsIn vivo, BTX-A attenuated chronic compression injury (CCI)-induced pain in rats, and reduced production of pro-inflammatory factors. The inhibition of BTX-A to expression and phosphorylation of SNAP23 were partly reversed by TLR2/MyD88 upregulation. In LPS-stimulated microglia, we also found that BTX-A suppressed TLR2, MyD88, p-SNAP23 and SNAP23 expression, and reduced pro-inflammatory factors secretion. Upregulation of TLR2 and MyD88 recued the inhibition of BTX-A to LPS-induced activation of SNAP23. Then, we demonstrated that BTX-A reduced expression of SNAP23 through inhibition of IKKα/β phosphorylation. Besides, the inhibition of BTX-A to LPS-induced upregulation of SNAP23 can be reversed by proteasome inhibitor. NEDD4, an E3 ubiquitin ligase, was proved to be bind with SNAP23. BTX-A reduced expression of SNAP23 via facilitating ubiquitin-mediated degradation of SNAP23.
conclusionOverall, our data demonstrated that BTX-A attenuated NP via reducing the secretion of pro-inflammatory factors from microglia by inhibition of TLR2/MyD88 signaling. BTX-A downregulated expression of SNAP23 via reducing phosphorylation of IKKα/β, and enhancing ubiquitination of SNAP23 by suppressing TLR2/MyD88 signaling.
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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.