ArticleCell & bioscience2020
Botulinum toxin type A promotes microglial M2 polarization and suppresses chronic constriction injury-induced neuropathic pain through the P2X7 receptor.
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 33 papers.
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Who cites it
33 citing papers in PubMed, 95 citations in OpenAlex.
- P2X7 Receptor as a Therapeutic Target for Neuropathic Pain: From Mechanisms to Translational Strategies.Current pain and headache reports · 2026Review
- The mechanism of dynamic switching between M1/M2 phenotypes of microglia in neuropathic pain: a narrative review.Frontiers in molecular neuroscience · 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
- Botulinum toxin type A inhibits chronic post-thoracotomy pain through the HMGB1-mediated TLR4/NF-κB signaling pathway.American journal of translational research · 2026Article
- PGC-1α Transcriptionally Regulated by ChREBP Mitigates Neuropathic Pain Through Promoting Microglial Fatty Acid Oxidation and Anti-Inflammatory Response.CNS neuroscience & therapeutics · 2026Article
- 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
- Mechanisms and Therapeutic Prospects of Microglia-Astrocyte Interactions in Neuropathic Pain Following Spinal Cord Injury.Molecular neurobiology · 2025Review
- Protective effect of lappaconitine on Freund's complete adjuvant-induced arthritis exerted through P2X7 receptor-mediated regulation of M1/M2 balance in rats.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Focus on P2X7R in microglia: its mechanism of action and therapeutic prospects in various neuropathic pain models.Frontiers in pharmacology · 2025Review
- FOXA2/miR-148a-3p/SMURF2 signaling feed-forward loop alleviates spinal cord ischemia-reperfusion injury-induced neuropathic pain by modulating microglia polarization in rats.Frontiers in immunology · 2025Article
- TRAF6 promotes spinal microglial M1 polarization to aggravate neuropathic pain by activating the c-JUN/NF-kB signaling pathway.Cell biology and toxicology · 2024Article
- Neurobiological mechanisms of botulinum neurotoxin-induced analgesia for neuropathic pain.Pharmacology & therapeutics · 2024Review
- Predicting Diagnostic Biomarkers Associated with Pyroptosis in Neuropathic Pain Based on Machine Learning and Experimental Validation.Journal of inflammation research · 2024Article
- Exploring the Biomarkers and Potential Mechanisms of Botulinum Toxin Type A in the Treatment of Microglial Inflammatory Activation through P2X7 Receptors based on Transcriptome Sequencing.Current pharmaceutical design · 2024Article
- Obacunone Alleviates Inflammatory Pain by Promoting M2 Microglial Polarization and by Activating Nrf2/HO-1 Signaling Pathway.Drug design, development and therapy · 2024Article
- Involvement of microglial P2X7 receptor in pain modulation.CNS neuroscience & therapeutics · 2024Review
- Three-dimensional human neural culture on a chip recapitulating neuroinflammation and neurodegeneration.Nature protocols · 2023Review
- Chinese Tuina remodels the synaptic structure in neuropathic pain rats by downregulating the expression of N-methyl D-aspartate receptor subtype 2B and postsynaptic density protein-95 in the spinal cord dorsal horn.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Microglia polarization in nociplastic pain: mechanisms and perspectives.Inflammopharmacology · 2023Review
- Emerging roles of the P2X7 receptor in cancer pain.Purinergic signalling · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSwitching microglial polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype represents a novel therapeutic strategy for neuropathic pain (NP). This study aims to investigate whether botulinum toxin type A (BTX-A) regulates microglial M1/M2 polarization by inhibiting P2X7 expression in a rat model of NP.
resultsThe BTX-A administration elevated pain threshold, induced microglial polarization toward the M2 phenotype, and decreased P2X7 protein level in a rat model of NP induced by chronic compression injury (CCI). Lipopolysaccharide (LPS) was used to activate HAPI rat microglial cells as an in vitro inflammatory model and we demonstrated that BTX-A promoted microglial M2 polarization in LPS-stimulated HAPI microglial cells through suppressing P2X7.
conclusionsOur results indicate that BTX-A promotes microglial M2 polarization and suppresses CCI-induced NP through inhibiting P2X7 receptor. These findings provide new insights into the mechanism of BTX-A in relieving NP.
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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.