ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
GDNF, Neurturin, and Artemin Activate and Sensitize Bone Afferent Neurons and Contribute to Inflammatory Bone Pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Recent research advances in pain mechanisms in McCune-Albright syndrome thinking about the pain mechanism of FD/MAS.Journal of orthopaedic surgery and research · 2024Pooled it
- Sensing the skeleton: sensorineural regulation in bone.Nature reviews. Neuroscience · 2026Review
- The Interaction Between the Central Nervous System and Dental Tissues: Hypothetical Dental Interoception Inferred From Skeletal Interoception.Journal of oral rehabilitation · 2026Review
- Recombinant Artemin-Fc Fusion Protein Attenuates TLR4/NF-κB-Associated Neuroinflammation and Modulates Inhibitory/Excitatory Synaptic Marker Expression After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- MAPK-dependent release of GDNF from Schwann cells mediates tumor-independent pain in neurofibromatosis 1.Science signaling · 2026Article
- Causal relationship between 91 circulating inflammatory proteins and osteomyelitis risk: evidence from a Mendelian randomization study.Archives of medical science : AMS · 2026Article
- Artemin/GFRA3 axis and TRP channels: molecular insights from a feline model of osteoarthritis.Frontiers in pain research (Lausanne, Switzerland) · 2026Article
- Methodological comparison between salivary and plasma inflammatory biomarkers in third molar surgery patients.BMC oral health · 2025Article
- Artemin sensitises mouse (Mus musculus) and naked mole-rat (Heterocephalus glaber) sensory neurons in vitro.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2025Article
- Review
- Article
- An in vivo electrophysiological preparation for mechanical, electrical and optical stimulation of sensory neurons that innervate murine bone.Animal models and experimental medicine · 2025Article
- Peripheral neuronal sensitization and neurovascular remodelling in osteoarthritis pain.Nature reviews. Rheumatology · 2025Review
- Ectopic Nociceptor Sprouting as a Key Peripheral Driver of Pain in Rheumatoid Arthritis.Current rheumatology reports · 2025Review
- Mechanism of Intervertebral Disc Degeneration via the β-Catenin/CCL2 Pathway in Sox9 Conditional Knockout Mice.JOR spine · 2025Article
- Emerging evidence of artemin/GFRα3 signaling in musculoskeletal pain.Osteoarthritis and cartilage · 2025Review
- ARTN and CCL23 predicted chemosensitivity in acute myeloid leukemia: an OlinkClinical proteomics · 2025Article
- A Procedural Overview of the Involvement of Small Molecules in the Nervous System in the Regulation of Bone Healing.International journal of nanomedicine · 2025Review
- Single-Cell Transcriptome Analyses of Four Pain Related Genes in Osteosarcoma.Cancer informatics · 2025Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pain associated with skeletal pathology or disease is a significant clinical problem, but the mechanisms that generate and/or maintain it remain poorly understood. In this study, we explored roles for GDNF, neurturin, and artemin signaling in bone pain using male Sprague Dawley rats. We have shown that inflammatory bone pain involves activation and sensitization of peptidergic, NGF-sensitive neurons via artemin/GDNF family receptor α-3 (GFRα3) signaling pathways, and that sequestering artemin might be useful to prevent inflammatory bone pain derived from activation of NGF-sensitive bone afferent neurons. In addition, we have shown that inflammatory bone pain also involves activation and sensitization of nonpeptidergic neurons via GDNF/GFRα1 and neurturin/GFRα2 signaling pathways, and that sequestration of neurturin, but not GDNF, might be useful to treat inflammatory bone pain derived from activation of nonpeptidergic bone afferent neurons. Our findings suggest that GDNF family ligand signaling pathways are involved in the pathogenesis of bone pain and could be targets for pharmacological manipulations to treat it.
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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 OpenQuestion graph.