Evidence map›Paper›PMID 39210150›Full record

ArticleNature aging2024

Ribosomal S6 kinase 1 regulates inflammaging via the senescence secretome.

Suchira Gallage, Elaine E Irvine, Jose Efren Barragan Avila, Virinder Reen, Silvia M A Pedroni, Imanol Duran, Vikas Ranvir, Sanjay Khadayate, Joaquim Pombo, Sharon Brookes and 9 more

Abstract read
In one paragraph

Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. An siRNA targetingMolecular therapy. Nucleic acids · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Senotherapy for chronic lung disease.Pharmacological reviews · 2025
    Review
  19. Review
  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

19 authors.

Suchira GallageMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.ORCID http://orcid.org/0000-0002-1956-3597
Elaine E IrvineMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Jose Efren Barragan AvilaDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-9348-909X
Virinder ReenMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Silvia M A PedroniMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Imanol DuranMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.ORCID http://orcid.org/0000-0001-6615-3788
Vikas RanvirEmmy Noether Research Group, Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Epigenetic Machineries and Cancer, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-0437-6908
Sanjay KhadayateMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.ORCID http://orcid.org/0000-0003-4278-6403
Joaquim PomboMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Sharon BrookesMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Danijela HeideDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Gopuraja DharmalinghamMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Agharul I ChoudhuryMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Indrabahadur SinghEmmy Noether Research Group, Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Epigenetic Machineries and Cancer, Heidelberg, Germany.
Nicolás HerranzMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.
Santiago VerniaMedical Research Council Laboratory of Medical Sciences (LMS), London, UK.ORCID http://orcid.org/0000-0001-6728-5555
Mathias HeikenwalderDivision of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg, Germany. m.heikenwaelder@dkfz-heidelberg.de.ORCID http://orcid.org/0000-0002-3135-2274
Jesús GilMedical Research Council Laboratory of Medical Sciences (LMS), London, UK. jesus.gil@imperial.ac.uk.ORCID http://orcid.org/0000-0002-4303-6260
Dominic J WithersMedical Research Council Laboratory of Medical Sciences (LMS), London, UK. d.withers@imperial.ac.uk.ORCID http://orcid.org/0000-0002-8009-7521

Funding

Cancer Research UK (CRUK) C15075/A28647EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) HepatoMetaboPathRCUK | Medical Research Council (MRC) MC_U120085810RCUK | MRC | Medical Research Foundation MC-A654-5QB40Wellcome TrustWellcome Trust (Wellcome) 098565/Z/12/Z
6 · The paper itself

Abstract

Inhibition of S6 kinase 1 (S6K1) extends lifespan and improves healthspan in mice, but the underlying mechanisms are unclear. Cellular senescence is a stable growth arrest accompanied by an inflammatory senescence-associated secretory phenotype (SASP). Cellular senescence and SASP-mediated chronic inflammation contribute to age-related pathology, but the specific role of S6K1 has not been determined. Here we show that S6K1 deletion does not reduce senescence but ameliorates inflammation in aged mouse livers. Using human and mouse models of senescence, we demonstrate that reduced inflammation is a liver-intrinsic effect associated with S6K deletion. Specifically, we show that S6K1 deletion results in reduced IRF3 activation; impaired production of cytokines, such as IL1β; and reduced immune infiltration. Using either liver-specific or myeloid-specific S6K knockout mice, we also demonstrate that reduced immune infiltration and clearance of senescent cells is a hepatocyte-intrinsic phenomenon. Overall, deletion of S6K reduces inflammation in the liver, suggesting that suppression of the inflammatory SASP by loss of S6K could underlie the beneficial effects of inhibiting this pathway on healthspan and lifespan.

Indexed as

Cellular SenescenceInflammationLiverMice, KnockoutRibosomal Protein S6 Kinases, 90-kDaAgingAnimalsHepatocytesHumansInterferon Regulatory Factor-3Interleukin-1betaMaleMiceSenescence-Associated Secretory PhenotypeInterferon Regulatory Factor-3Interleukin-1betaRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouse

Identifiers

PMID39210150
PMCPMC11564105

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Registered trials

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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.