ArticlePain reports
Spinal microglia contribute to cancer-induced pain through system x
Article in Pain reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Proteomic Adaptations in the Spinal Cord of a Breast Cancer Model of Paclitaxel-Induced Peripheral Neuropathy.Journal of proteome research · 2026Article
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- Recent advances in potential therapeutic targets of ferroptosis‑associated pathways for the treatment of stroke (Review).Molecular medicine reports · 2024Review
- Implication of system xJournal of neuroinflammation · 2024Article
- Glutamatergic systems in neuropathic pain and emerging non-opioid therapies.Pharmacological research · 2022Review
- Potential therapeutic treatments of cancer-induced bone pain.Current opinion in supportive and palliative care · 2020Review
- RETRACTED: Ultramicronized Palmitoylethanolamide and Paracetamol, a New Association to Relieve Hyperalgesia and Pain in a Sciatic Nerve Injury Model in Rat.International journal of molecular sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMicroglial cells, the resident macrophages of the central nervous system, are a key contributor to the generation and maintenance of cancer-induced pain (CIP). In healthy organisms, activated microglia promote recovery through the release of trophic and anti-inflammatory factors to clear toxins and pathogens and support neuronal survival. Chronically activated microglia, however, release toxic substances, including excess glutamate, causing cytotoxicity. Accordingly, rising attention is given to microglia for their role in abnormal physiology and in mediating neurotoxicity.
objectivesTo examine the nociceptive relationship between peripherally-released glutamate and microglial xCT.
methodsA validated murine model of 4T1 carcinoma cell-induced nociception was used to assess the effect of peripheral tumour on spinal microglial activation and xCT expression. Coculture systems were then used to investigate the direct effect of glutamate released by wildtype and xCT knockdown MDA-MB-231 carcinoma cells on microglial activation, functional system x
resultsBlockade of system x
conclusionsThese data collectively demonstrate that the system xCT antiporter is functionally implicated in CIP and may be particularly relevant to pain progression through microglia. Upregulated xCT in chronically activated spinal microglia may be one pathway to central glutamate cytotoxicity. Microglial xCT may therefore be a valuable target for mitigating CIP.
Indexed as
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What OpenQuestion holds
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.