ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
Activation of the STING pathway induces peripheral sensitization via neuroinflammation in a rat model of bone cancer pain.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Microglial MARCO facilitates Varicella zoster virus uptake and triggers TLR2-mediated neuroinflammation.Journal of biomedical science · 2026Article
- Mitochondrial DNA release contributes to neuropathic pain via a cGAS-STING-IRF3-CMPK2-associated immunometabolic feedback mechanism.Journal of translational medicine · 2026Article
- Remimazolam Ameliorates Autistic-Like Behaviors via Suppression of Ferroptosis in VTA Dopaminergic Neurons in a Mouse Model of ASD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Spinal KCC2 Mediates the Modulation Effect of HDAC2 on Bone Cancer Pain in Rats.Current cancer drug targets · 2026Article
- The research progress into cellular mechanosensitive ion channels mediating cancer pain.Channels (Austin, Tex.) · 2025Review
- Breaking barriers: The cGAS-STING pathway as a novel frontier in cancer immunotherapy.Cancer communications (London, England) · 2025Review
- Synergistic Inhibition of Nav1.7 and NCX1: A Novel Strategy for Treating Cancer-Induced Bone Pain by Modulating Pain Sensitization and Neuronal Inflammation.CNS neuroscience & therapeutics · 2025Article
- Recent advancements in cGAS-STING activation, tumor immune evasion, and therapeutic implications.Medical oncology (Northwood, London, England) · 2024Review
- STING mediates microglial pyroptosis via interaction with NLRP3 in cerebral ischaemic stroke.Stroke and vascular neurology · 2024Article
- Emerging Molecular and Synaptic Targets for the Management of Chronic Pain Caused by Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- Vinorelbine causes a neuropathic pain-like state in mice via STING and MNK1 signaling associated with type I interferon induction.iScience · 2024Article
- Exploring blood transcriptomic signatures in patients with herpes zoster and postherpetic neuralgia.Frontiers in cellular and infection microbiology · 2024Article
- Immunotherapies in chronic pain through modulation of neuroimmune interactions.Pharmacology & therapeutics · 2023Review
- TET1-TRPV4 Signaling Contributes to Bone Cancer Pain in Rats.Brain sciences · 2023Article
- Potential Therapeutic Value of the STING Inhibitors.Molecules (Basel, Switzerland) · 2023Review
- Mechanism and effects of STING-IFN-I pathway on nociception: A narrative review.Frontiers in molecular neuroscience · 2022Review
- Article
- Mitochondrial DAMPs produce inflammatory hyperalgesia via stimulator of interferon genes (STING) activation in DRG neurons.Molecular painArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNeuroinflammation in the peripheral nervous system has been linked to cancer metastasis-induced bone pain. The stimulator of interferon genes (STING), an innate immune sensor for cytosolic DNA, plays an important role in inflammation and cancer metastasis and is reported to be a critical regulator of nociception. Here, we examined the role of STING in primary nociceptive neurons and chronic pain to determine if it could be a new target for treating bone cancer pain (BCP).
methodsWalker 256 cancer cells were injected intratibially to induce bone cancer pain in rats. STING and its downstream inflammatory factors in dorsal root ganglia (DRG) were detected using western blotting and immunofluorescent staining. Transmission electron microscopy and the BCL2-associated X (Bax) expression were used to detect the mitochondrial stress in DRG neurons. C-176, a specific inhibitor of STING, was used to block STING activation and to test the pain behavior.
resultsMechanical hyperalgesia and spontaneous pain were observed in BCP rats, accompanied by the upregulation of the STING expression in the ipsilateral L4-5 DRG neurons which showed significant mitochondrion stress. The STING/TANK-binding kinase 1 (TBK1)/nuclear factor-kappa B (NF-κB) pathway activation was observed in the DRGs of BCP rats as well as increased IL-1β, IL-6, and TNF-α expression. C-176 alleviated bone cancer pain and reduced the STING and its downstream inflammatory pathway.
conclusionWe provide evidence that STING pathway activation leads to neuroinflammation and peripheral sensitization. Pharmacological blockade of STING may be a promising novel strategy for preventing BCP.
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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.