ArticleGlia2017
Complement 3a receptor in dorsal horn microglia mediates pronociceptive neuropeptide signaling.
Article in Glia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Molecular basis of diverse ligand recognition and species-specific pharmacology at the complement anaphylatoxin receptor C3aR.Nature communications · 2026Article
- Complement 3a Receptor mediates high fat diet induced hypothalamic accumulation of lipid associated microglia to regulate neuroinflammation and obesity.bioRxiv : the preprint server for biology · 2026Article
- A Novel Class of Complement 3a Receptor Agonists and Antagonists Derived from the TLQP-21 Peptide.Journal of medicinal chemistry · 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
- Single-cell transcriptome atlas of spontaneous dry age-related macular degeneration in macaques.Fundamental research · 2025Article
- Complement C3aR signaling: Immune and metabolic modulation and its impact on Alzheimer's disease.European journal of immunology · 2024Review
- The complement system: a potential target for the comorbidity of chronic pain and depression.The Korean journal of pain · 2024Article
- P2RY13 is a prognostic biomarker and associated with immune infiltrates in renal clear cell carcinoma: A comprehensive bioinformatic study.Health science reports · 2023Article
- TLQP-21 is a low potency partial C3aR activator on human primary macrophages.Frontiers in immunology · 2023Article
- Shared Genetic Regulatory Networks Contribute to Neuropathic and Inflammatory Pain: Multi-Omics Systems Analysis.Biomolecules · 2022Article
- Thalamocortical axons regulate neurogenesis and laminar fates in the early sensory cortex.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification of hub genes and immune cell infiltration characteristics in chronic rhinosinusitis with nasal polyps: Bioinformatics analysis and experimental validation.Frontiers in molecular biosciences · 2022Article
- The molecular identity of the TLQP-21 peptide receptor.Cellular and molecular life sciences : CMLS · 2021Review
- Targeting Complement C3a Receptor to Improve Outcome After Ischemic Brain Injury.Neurochemical research · 2021Review
- Article
- Review
- Stress and Alzheimer's disease: A senescence link?Neuroscience and biobehavioral reviews · 2020Review
- VGF-derived peptide TLQP-21 modulates microglial function through C3aR1 signaling pathways and reduces neuropathology in 5xFAD mice.Molecular neurodegeneration · 2020Article
- Insights Into Spinal Dorsal Horn Circuit Function and Dysfunction Using Optical Approaches.Frontiers in neural circuits · 2020Review
- Peptide/Receptor Co-evolution Explains the Lipolytic Function of the Neuropeptide TLQP-21.Cell reports · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The complement 3a receptor (C3aR1) participates in microglial signaling under pathological conditions and was recently shown to be activated by the neuropeptide TLQP-21. We previously demonstrated that TLQP-21 elicits hyperalgesia and contributes to nerve injury-induced hypersensitivity through an unknown mechanism in the spinal cord. Here we determined that this mechanism requires C3aR1 and that microglia are the cellular target for TLQP-21. We propose a novel neuroimmune signaling pathway involving TLQP-21-induced activation of microglial C3aR1 that then contributes to spinal neuroplasticity and neuropathic pain. This unique dual-ligand activation of C3aR1 by a neuropeptide (TLQP-21) and an immune mediator (C3a) represents a potential broad-spectrum mechanism throughout the CNS for integration of neuroimmune crosstalk at the molecular level.
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Identifiers
What Socratic holds
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.