ArticleLife (Basel, Switzerland)2023
Electroacupuncture Attenuates Fibromyalgia Pain via Toll-like Receptor 4 in the Mouse Brain.
Article in Life (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanisms of Different Brainstem Nuclei Involved in Electroacupuncture-Induced Analgesia.Chinese journal of integrative medicine · 2026Review
- Therapeutic and research frontiers in fibromyalgia: integrating pathophysiology with innovative drug repurposing.Inflammopharmacology · 2026Review
- Moving Toward Objective Diagnosis in Fibromyalgia: Emerging Biomarkers and Digital Phenotyping Tools.Biomedicines · 2026Review
- Article
- Microglia's Phenotypic Heterogeneity in Pain Pathogenesis and Electroacupuncture Analgesia: Mechanisms and Therapeutic Potential.Journal of pain research · 2025Review
- Electroacupuncture Reduced Fibromyalgia-Pain-like Behavior through Inactivating Transient Receptor Potential V1 and Interleukin-17 in Intermittent Cold Stress Mice Model.Brain sciences · 2024Article
- Degree centrality-based resting-state functional magnetic resonance imaging explores central mechanisms in lumbar disc herniation patients with chronic low back pain.Frontiers in neurology · 2024Article
- Therapeutic modulation of pain-related affective disorders by acupuncture: Mechanistic review.Molecular painReview
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundFibromyalgia (FM) is characterized by complex pain symptoms lacking impersonal considerations in diagnosis and treatment evaluation, which often happens in women. Chronic and persistent widespread pain is the key symptom disturbing patients with FM, leading to depression, obesity, and sleep disturbances. Toll-like receptor 4 (TLR4) activation produces a harmful sensory input involved in central pain; this is the focus of this study. Electroacupuncture (EA) has beneficial effects in reducing FM pain, but its connection with TLR4 signaling is still unknown.
methodsIntermittent cold stress significantly induced mechanical and thermal pain. EA, but not sham EA, reliably attenuated mechanical and thermal hyperalgesia. The increased inflammatory mediators in FM mice were reduced in the EA group, but not in the sham group.
resultsAll TLR4 and related molecule levels increased in the FM mice's hypothalamus, periaqueductal gray (PAG), and cerebellum. These increases could be attenuated by EA but not sham stimulation. Activation of TLR4 by lipopolysaccharide (LPS) significantly induced FM and can be further reversed by a TLR4 antagonist.
conclusionsThese mechanisms provide evidence that the analgesic effect of EA is related to the TLR4 pathway. In addition, we showed that inflammation can activate the TLR4 pathway and provided new possible therapeutic targets for FM pain.
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