Evidence map›Paper›PMID 24960204›Full record

ArticleNature communications2014

Chronic inflammation induces telomere dysfunction and accelerates ageing in mice.

Diana Jurk, Caroline Wilson, João F Passos, Fiona Oakley, Clara Correia-Melo, Laura Greaves, Gabriele Saretzki, Chris Fox, Conor Lawless, Rhys Anderson and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 443 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
443citing papers in PubMed, 3 pooled it
31.6field-weighted citation impact, top 1% 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

443 citing papers in PubMed, 3 syntheses or guidelines pooled it, 776 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Telomere Length and Hearing Loss: A Two-Sample Mendelian Randomization.International journal of environmental research and public health · 2022
    Pooled it
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Mice lacking NF-ĸB1 undergo premature ovarian aging.Reproductive biology and endocrinology : RB&E · 2026
    Article
  12. Observational
  13. Review
  14. Review
  15. Review
  16. Article
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  18. Article
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383 more citing papers are in PubMed but not listed here.

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

18 authors at 3 institutions in 2 countries.

Diana JurkInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Caroline WilsonFibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
João F PassosInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Fiona OakleyFibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Clara Correia-MeloInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Laura GreavesMitochondrial Research Group, Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Gabriele SaretzkiInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Chris FoxFibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Conor Lawless1] Institute for Ageing and Health, Newcastle University, NE4 5PL, UK [2] Institute for Cell and Molecular Biosciences, Newcastle University, Catherine Cookson Building, Framlington Place, Newcastle Upon Tyne NE2 4HH, UK.
Rhys AndersonInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Graeme HewittInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Sylvia Lf PenderFaculty of Medicine, University of Southampton. Mailpoint 813, Sir Henry Wellcome Laboratories, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK.
Nicola FullardFibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Glyn NelsonInstitute for Ageing and Health, Newcastle University, NE4 5PL, UK.
Jelena MannFibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK.
Bart van de SluisMolecular Genetics Laboratory, Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, 9713 AV Groningen, The Netherlands.
Derek A Mann1] Fibrosis Laboratory, Liver Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne NE2 4HH, UK [2].
Thomas von Zglinicki1] Institute for Ageing and Health, Newcastle University, NE4 5PL, UK [2].
Newcastle University · GBSouthampton General Hospital · GBUniversity of Groningen · NL

Funding

Biotechnology and Biological Sciences Research Council BB/C008200/1Biotechnology and Biological Sciences Research Council BB/F010966/1Biotechnology and Biological Sciences Research Council BB/H022384/1Biotechnology and Biological Sciences Research Council BB/I020748/1Medical Research Council G0700718Medical Research Council G0700890Medical Research Council G0900535Medical Research Council MK/K001949/1Medical Research Council MR/K001949/1Medical Research Council MR/L016354/1National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/K000748/1Wellcome TrustWellcome Trust WT084961MA
6 · The paper itself

Abstract

Chronic inflammation is associated with normal and pathological ageing. Here we show that chronic, progressive low-grade inflammation induced by knockout of the nfkb1 subunit of the transcription factor NF-κB induces premature ageing in mice. We also show that these mice have reduced regeneration in liver and gut. nfkb1(-/-) fibroblasts exhibit aggravated cell senescence because of an enhanced autocrine and paracrine feedback through NF-κB, COX-2 and ROS, which stabilizes DNA damage. Preferential accumulation of telomere-dysfunctional senescent cells in nfkb1(-/-) tissues is blocked by anti-inflammatory or antioxidant treatment of mice, and this rescues tissue regenerative potential. Frequencies of senescent cells in liver and intestinal crypts quantitatively predict mean and maximum lifespan in both short- and long-lived mice cohorts. These data indicate that systemic chronic inflammation can accelerate ageing via ROS-mediated exacerbation of telomere dysfunction and cell senescence in the absence of any other genetic or environmental factor.

Indexed as

Aging, PrematureAnimalsCellular SenescenceChronic DiseaseCyclooxygenase 2DNA DamageFeedback, PhysiologicalFibroblastsInflammationLiver RegenerationMiceMice, KnockoutNF-kappa BNF-kappa B p50 SubunitReactive Oxygen SpeciesRegenerationCyclooxygenase 2NF-kappa BNF-kappa B p50 SubunitNfkb1 protein, mousePtgs2 protein, ratReactive Oxygen Species

Identifiers

PMID24960204
PMCPMC4090717
OpenAlexW2125764628

What OpenQuestion holds

Textmetadata
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.