ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
GPR37 Activation Alleviates Bone Cancer Pain via the Inhibition of Osteoclastogenesis and Neuronal Hyperexcitability.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Bioactive polythioctic acid-engineered ropivacaine alleviates bone cancer pain through prolonged analgesia and multi-functional neuroprotection.Materials today. Bio · 2026Article
- Cancer-related pain: A bidirectional modulator of cancer progression.Clinical and translational medicine · 2026Review
- GPR37 activation erases spinal pain memory and resolves increased nociception in murine models.bioRxiv : the preprint server for biology · 2025Article
- Neuroprotectin D1 and GPR37 protect against chemotherapy-induced peripheral neuropathy and the transition from acute to chronic pain.Pharmacological research · 2025Article
- GPR37 Activation Alleviates Bone Cancer Pain via the Inhibition of Osteoclastogenesis and Neuronal Hyperexcitability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neurotrophic factors as double-edged swords in osteosarcoma: drivers of tumour growth and immune remodelling.Frontiers in immunology · 2025Review
- Role and regulatory mechanism of GPR37 in neurological diseases.Frontiers in cellular neuroscience · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
Osteolytic bone cancer pain is a primary concern for cancer patients with bone metastasis, and current therapies offer inadequate pain relief. The present study demonstrates that activation of the G protein-coupled receptor 37 (GPR37) by neuroprotectin D1 (NPD1) or artesunate (ARU) alleviates both acute and persistent pain in multiple mouse models of bone cancer. GPR37 agonists also protect against cancer-induced bone destruction. Mechanistically, NPD1 or ARU binding to GPR37 in macrophages promotes the release of IL-10, which further inhibits cancer-induced osteoclastogenesis. Moreover, direct activation of GPR37 in dorsal root ganglion (DRG) neurons and the spinal dorsal horn reduces action potential firing and the frequency of spontaneous excitatory postsynaptic currents (sEPSCs), thereby suppressing cancer-induced neuronal hyperexcitability. Importantly, the analgesic and protective effects of NPD1 and ARU are abolished in Gpr37
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