ArticleNature communications2024
Schwann cell C5aR1 co-opts inflammasome NLRP1 to sustain pain in a mouse model of endometriosis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed.
- Review
- Targeting the Immune Network in Endometriosis: A Comprehensive Review of Pathogenesis, Immunomodulation, and Emerging Therapies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Decoding the Histomorphological and Multi-Omic Characteristics of Melanotic Schwannoma.Current medical science · 2026Article
- Biphasic modulation of large-fiber excitability accompanied by dynamic nerve-intrinsic immune activation following CFA-induced peripheral inflammation in mice.Scientific reports · 2026Article
- Schwann Cell TRPA1, a Proalgesic Ion Channel, Mediates Neuroinflammation and Fibromyalgia-Associated Behaviours in Mice.Journal of neurochemistry · 2026Review
- Roles of the Complement System in Peripheral Nerve Injury and Repair.Bioengineering (Basel, Switzerland) · 2026Review
- Targeting glial-orchestrated neuroinflammation in migraine pathophysiology.The journal of headache and pain · 2026Review
- Electroacupuncture ameliorates incisional pain via suppressing IL-33 signaling-related macrophage infiltration and ROS overproduction in incised skin.Chinese medicine · 2026Article
- Complement and inflammasome crosstalk in chronic inflammation.Frontiers in immunology · 2026Review
- Inflammasomes meet organoids and artificial intelligence: unraveling the complexity of gynecological inflammation.Frontiers in immunology · 2026Review
- Schwann cell Lrp1 deletion drives trigeminal neuron sensitization and orofacial pain by modulating mitochondrial function and TRPV1/TRPA1 activity.The journal of headache and pain · 2025Article
- Precision Therapeutic and Preventive Molecular Strategies for Endometriosis-Associated Infertility.International journal of molecular sciences · 2025Review
- Investigating the impact of selegiline on the NF-kB/NLRP3/Caspase-1 signaling pathway in A549 lung epithelial cells exposed to lipopolysaccharide.Cytotechnology · 2025Article
- Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large-Caliber Fibers in Mice.Journal of neurochemistry · 2025Article
- Unveiling the Mechanisms of Pain in Endometriosis: Comprehensive Analysis of Inflammatory Sensitization and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Glycine attenuates sepsis-induced white matter injury by modulating gut microbiota.Frontiers in molecular biosciences · 2025Article
- Dual role of complement in neuronal repair.Frontiers in immunology · 2025Review
- Update on the pathogenesis of endometriosis-related infertility based on contemporary evidence.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
Over 60% of women with endometriosis experience abdominopelvic pain and broader pain manifestations, including chronic back pain, fibromyalgia, chronic fatigue, vulvodynia, and migraine. Although the imbalance of proinflammatory mediators, including the complement component C5a, is associated with endometriosis-related pain, the mechanisms causing widespread pain and the C5a role remain unclear. Female mice and women with endometriosis exhibit increased plasma C5a levels and pain. We hypothesize the Schwann cells involvement in endometriotic pain. Here, we show that silencing the C5a receptor (C5aR1) in Schwann cells blocks the C5a-induced activation of the NLRP1 inflammasome and subsequent release of interleukin-1β (IL-1β). Macrophages, recruited to sciatic/trigeminal nerves by IL-1β from Schwann cells, increase oxidative stress, which activates the proalgesic TRPA1 pathway, resulting in widespread pain. These findings reveal a pathway involving Schwann cell C5aR1, NLRP1/IL-1β activation, macrophage recruitment, oxidative stress, and TRPA1 engagement, contributing to pain in a mouse model of endometriosis.
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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.