ArticleiScience2024
Oleic acid released by sensory neurons inhibits TRPV1-mediated thermal hypersensitivity via GPR40.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Exploring GC-MS-Based Phytochemistry and Network Pharmacology to Elucidate the Multi-Target Therapeutic Potential of Betel Leaf Oil as an Analgesic and Anti-Inflammatory Agent.Biomedical chromatography : BMC · 2026Article
- Review
- Topical oleic acid reduces nociception and inflammation in a UVB radiation-induced sunburn model in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Metabolite-Sensing Receptors: Emerging Targets for Modulating Chronic Pain Pathways.Current issues in molecular biology · 2025Review
- Bioactive lipid signaling and lipidomics in macrophage polarization: Impact on inflammation and immune regulation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Noxious stimuli activate nociceptive sensory neurons, causing action potential firing and the release of diverse signaling molecules. Several peptides have already been identified to be released by sensory neurons and shown to modulate inflammatory responses and inflammatory pain. However, it is still unclear whether lipid mediators can be released upon sensory neuron activation to modulate intercellular communication. Here, we analyzed the lipid secretome of capsaicin-stimulated nociceptive neurons with LC-HRMS, revealing that oleic acid is strongly released from sensory neurons by capsaicin. We further demonstrated that oleic acid inhibits capsaicin-induced calcium transients in sensory neurons and reverses bradykinin-induced TRPV1 sensitization by a calcineurin (CaN) and GPR40 (FFAR1) dependent pathway. Additionally, oleic acid alleviated zymosan-mediated thermal hypersensitivity via the GPR40, suggesting that the capsaicin-mediated oleic acid release from sensory neurons acts as a protective and feedback mechanism, preventing sensory neurons from nociceptive overstimulation via the GPR40/CaN/TRPV1-axis.
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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.