Evidence map›Paper›PMID 40490553›Full record

ArticleThe EMBO journal2025

cGAS-STING are responsible for premature aging of telomerase-deficient zebrafish.

Naz Şerifoğlu, Giulia Allavena, Bruno Lopes-Bastos, Marta Marzullo, Andreia Marques, Pauline Colibert, Pavlos Bousounis, Eirini Trompouki, Miguel Godinho Ferreira

Abstract read
In one paragraph

Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. The inflammatory clock: how cGAS-STING ticks in the aging ovary.Frontiers in cell and developmental biology · 2026
    Review
  13. Review
  14. 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

9 authors.

Naz ŞerifoğluInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.
Giulia AllavenaInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.ORCID http://orcid.org/0000-0003-3267-175X
Bruno Lopes-BastosInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.
Marta MarzulloInstituto Gulbenkian de Ciência, Oeiras, Portugal.ORCID http://orcid.org/0000-0001-7229-1693
Andreia MarquesInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.ORCID http://orcid.org/0000-0001-9995-2500
Pauline ColibertInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.ORCID http://orcid.org/0009-0005-2880-3141
Pavlos BousounisDepartment of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Eirini TrompoukiInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France.
Miguel Godinho FerreiraInstitute for Research on Cancer and Aging of Nice (IRCAN), CNRS UMR7284, INSERM U1081, Université Cote d'Azur, 06107, Nice, France. Miguel-Godinho.FERREIRA@unice.fr.ORCID http://orcid.org/0000-0002-8363-7183

Funding

Agence Nationale de la Recherche ANR-21-CE14-0054French government, through the France 2030 investment plan managed by the Agence Nationale de la Recherche, as part of the Université Côte d'Azur's Initiative of Excellence ANR-15-IDEX-01German Research Foundation 322977937/GRK2344Institut National Du Cancer (INCa) PLBIO21-228La Ligue Contre le Cancer Bourse de DoctoratUniversite Cote dazur - Academie 4 Action 2
6 · The paper itself

Abstract

Telomere shortening occurs in multiple tissues throughout aging. When telomeres become critically short, they trigger DNA-damage responses and p53 stabilization, leading to apoptosis or replicative senescence. In vitro, cells with short telomeres activate the cGAS-STING innate immune pathway resulting in type-I interferon-based inflammation and senescence. However, the consequences of these events for the organism are not yet understood. Here, we show that sting is responsible for premature aging of telomerase-deficient zebrafish. We generated sting-/- tert-/- double-mutant animals and observed a thorough rescue of tert-/- phenotypes. At the cellular level, lack of cGAS-STING in tert mutants resulted in reduced senescence, increased cell proliferation, and decreased inflammation despite similarly short telomeres. Critically, absence of sting function resulted in dampening of the DNA damage response and reduced p53 levels. At the organism level, sting-/- tert-/- zebrafish regained fertility, showed delayed cachexia, and decreased cancer incidence, resulting in increased healthspan and lifespan of telomerase mutant animals.

Indexed as

Aging, PrematureMembrane ProteinsNucleotidyltransferasesTelomeraseZebrafishZebrafish ProteinsAnimalsDNA DamageTumor Suppressor Protein p53Membrane ProteinsNucleotidyltransferasesTelomeraseTumor Suppressor Protein p53Zebrafish ProteinsAgingcGAS-STINGInflammationTelomeraseZebrafish

Identifiers

PMID40490553
PMCPMC12402478

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.