Evidence map›Paper›PMID 38690737›Full record

ArticleThe Journal of clinical investigation2024

Induction of antiviral interferon-stimulated genes by neuronal STING promotes the resolution of pain in mice.

Manon Defaye, Amyaouch Bradaia, Nasser S Abdullah, Francina Agosti, Mircea Iftinca, Mélissa Delanne-Cuménal, Vanessa Soubeyre, Kristofer Svendsen, Gurveer Gill, Aye Ozmaeian and 10 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  10. Article
  11. Article
  12. Neuronal ALKAL2 and its ALK receptor contribute to the development of colitis-associated colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. STINGing away the pain: the role of interferon-stimulated genes.The Journal of clinical investigation · 2024
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 6 institutions in 3 countries.

Manon DefayeDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Amyaouch BradaiaDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Nasser S AbdullahDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Francina AgostiDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Mircea IftincaDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Mélissa Delanne-CuménalDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Vanessa SoubeyreDepartment of Neurosurgery, Gui de Chauliac Hospital, Donation and Transplantation Coordination Unit, Montpellier University Medical Center, Montpellier, France.
Kristofer SvendsenDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Gurveer GillDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Aye OzmaeianDepartment of Physiology and Pharmacology, Cumming School of Medicine.
Nadine GhezielToulouse Institute for Infectious and Inflammatory Diseases (INFINITy), INSERM UMR1291, University of Toulouse III, Toulouse, France.
Jérémy MartinToulouse Institute for Infectious and Inflammatory Diseases (INFINITy), INSERM UMR1291, University of Toulouse III, Toulouse, France.
Gaetan PoulenDepartment of Neurosurgery, Gui de Chauliac Hospital, Donation and Transplantation Coordination Unit, Montpellier University Medical Center, Montpellier, France.
Nicolas LonjonDepartment of Neurosurgery, Gui de Chauliac Hospital, Donation and Transplantation Coordination Unit, Montpellier University Medical Center, Montpellier, France.
Florence Vachiery-LahayeDepartment of Neurosurgery, Gui de Chauliac Hospital, Donation and Transplantation Coordination Unit, Montpellier University Medical Center, Montpellier, France.
Luc BauchetDepartment of Neurosurgery, Gui de Chauliac Hospital, Donation and Transplantation Coordination Unit, Montpellier University Medical Center, Montpellier, France.
Lilian BassoToulouse Institute for Infectious and Inflammatory Diseases (INFINITy), INSERM UMR1291, University of Toulouse III, Toulouse, France.
Emmanuel BourinetInstitute of Functional Genomics, Montpellier University, CNRS, INSERM, Montpellier, France.
Isaac M ChiuDepartment of Immunology, Blavatnik Institute, Harvard Medical School, Boston, Massachusetts, USA.
Christophe AltierDepartment of Physiology and Pharmacology, Cumming School of Medicine.
University of Calgary · CAUniversité de Montpellier · FRUniversité Toulouse III - Paul Sabatier · FRCentre National de la Recherche Scientifique · FRHarvard University · USResearch Network (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and pain are intertwined responses to injury, infection, or chronic diseases. While acute inflammation is essential in determining pain resolution and opioid analgesia, maladaptive processes occurring during resolution can lead to the transition to chronic pain. Here we found that inflammation activates the cytosolic DNA-sensing protein stimulator of IFN genes (STING) in dorsal root ganglion nociceptors. Neuronal activation of STING promotes signaling through TANK-binding kinase 1 (TBK1) and triggers an IFN-β response that mediates pain resolution. Notably, we found that mice expressing a nociceptor-specific gain-of-function mutation in STING exhibited an IFN gene signature that reduced nociceptor excitability and inflammatory hyperalgesia through a KChIP1-Kv4.3 regulation. Our findings reveal a role of IFN-regulated genes and KChIP1 downstream of STING in the resolution of inflammatory pain.

Indexed as

Membrane ProteinsNociceptorsAnimalsGanglia, SpinalInflammationInterferon-betaMaleMicePainProtein Serine-Threonine KinasesSignal TransductionSTING ProteinInterferon-betaMembrane ProteinsProtein Serine-Threonine KinasesSting1 protein, mouseSTING ProteinTbk1 protein, mouseInflammationInnate immunityIon channelsNeurosciencePain

Identifiers

PMID38690737
PMCPMC11060736
OpenAlexW4396530381

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.