ArticleCells2020
The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A Bibliometric Analysis of Publications on Macrophages in Peripheral Nerve Injury.Cellular and molecular neurobiology · 2026Article
- International Union of Basic and Clinical Pharmacology. CXXII. Applying an objective evaluation to the status of class A orphan G protein-coupled receptors.Pharmacological reviews · 2026Review
- Effects of Chlorogenic Acid on Deoxynivalenol (DON)-Induced Ferroptosis in Porcine Alveolar Macrophages.Toxins · 2026Article
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- pH sensing and inflammation: linking acidic microenvironments to immune reprogramming.Frontiers in immunology · 2026Review
- Prognostic significance of GPR132 in papillary thyroid carcinoma: insights from integrated machine learning and its role in regulating TPC-1 cell growth.Discover oncology · 2025Article
- Altered aminoacid and lipid metabolism in a rat orofacial inflammation model determined by omics approach: potential role in trigeminal sensitisation.The journal of headache and pain · 2025Article
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
- The Octadecanoids: Synthesis and Bioactivity of 18-Carbon Oxygenated Fatty Acids in Mammals, Bacteria, and Fungi.Chemical reviews · 2025Review
- The role and mechanisms of matrix metalloproteinase-9 in peripheral neuropathic pain.Frontiers in molecular neuroscience · 2025Review
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Endogenous Derivatives of Linoleic Acid and their Stable Analogs Are Potential Pain Mediators.JID innovations : skin science from molecules to population health · 2023Article
- Article
- Loss of the mammalian G-protein coupled receptor, G2A, modulates severity of invasive pulmonary aspergillosis.Frontiers in immunology · 2023Article
- Activation of orphan receptor GPR132 induces cell differentiation in acute myeloid leukemia.Cell death & disease · 2022Article
- Lysophosphatidylcholine: Potential Target for the Treatment of Chronic Pain.International journal of molecular sciences · 2022Review
- Iron Metabolism and Ferroptosis in Peripheral Nerve Injury.Oxidative medicine and cellular longevity · 2022Review
- Profiling of fatty acid metabolism in the dorsal root ganglion after peripheral nerve injury.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve injury-induced neuropathic pain is difficult to treat and mechanistically characterized by strong neuroimmune interactions, involving signaling lipids that act via specific G-protein coupled receptors. Here, we investigated the role of the signaling lipid receptor G2A (GPR132) in nerve injury-induced neuropathic pain using the robust spared nerve injury (SNI) mouse model. We found that the concentrations of the G2A agonist 9-HODE (9-Hydroxyoctadecadienoic acid) are strongly increased at the site of nerve injury during neuropathic pain. Moreover, G2A-deficient mice show a strong reduction of mechanical hypersensitivity after nerve injury. This phenotype is accompanied by a massive reduction of invading macrophages and neutrophils in G2A-deficient mice and a strongly reduced release of the proalgesic mediators TNFα, IL-6 and VEGF at the site of injury. Using a global proteome analysis to identify the underlying signaling pathways, we found that G2A activation in macrophages initiates MyD88-PI3K-AKT signaling and transient MMP9 release to trigger cytoskeleton remodeling and migration. We conclude that G2A-deficiency reduces inflammatory responses by decreasing the number of immune cells and the release of proinflammatory cytokines and growth factors at the site of nerve injury. Inhibiting the G2A receptor after nerve injury may reduce immune cell-mediated peripheral sensitization and may thus ameliorate neuropathic pain.
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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.