Evidence map›Paper›PMID 24011075›Full record

ArticleCell metabolism2013

DNA damage triggers a chronic autoinflammatory response, leading to fat depletion in NER progeria.

Ismene Karakasilioti, Irene Kamileri, Georgia Chatzinikolaou, Theodoros Kosteas, Eleni Vergadi, Andria Rasile Robinson, Iannis Tsamardinos, Tania A Rozgaja, Sandra Siakouli, Christos Tsatsanis and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

83 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular evolution of animal aging.The EMBO journal · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. SUL-138 mitigates accelerated endothelial aging and protects the kidney.Clinical science (London, England : 1979) · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Microglia-derived extracellular vesicles trigger age-related neurodegeneration upon DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Review
  18. Article
  19. Article
  20. Article

23 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

12 authors at 4 institutions in 2 countries.

Ismene KarakasiliotiInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, 70013 Heraklion, Crete, Greece; Department of Biology, University of Crete, 71409 Heraklion, Crete, Greece.
Irene Kamileri
Georgia Chatzinikolaou
Theodoros Kosteas
Eleni Vergadi
Andria Rasile Robinson
Iannis Tsamardinos
Tania A Rozgaja
Sandra Siakouli
Christos Tsatsanis
Laura J Niedernhofer
George A Garinis
University of Crete · GRFoundation for Research and Technology Hellas · GRScripps Research Institute · USUPMC Hillman Cancer Center · US

Funding

PROTEOMICSP01AG043376 · NIA · UNIVERSITY OF MINNESOTA · PI ROBBINS, PAUL D. · 2013 to 2019
$11.2M
The contribution of DNA interstrand crosslinks to agingR01ES016114 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIEDERNHOFER, LAURA JANE · 2007 to 2011
$2.5M
NIA NIH HHS P01 AG043376NIEHS NIH HHS ES016114NIEHS NIH HHS R01 ES016114
6 · The paper itself

Abstract

Lipodystrophies represent a group of heterogeneous disorders characterized by loss of fat tissue. However, the underlying mechanisms remain poorly understood. Using mice carrying an ERCC1-XPF DNA repair defect systematically or in adipocytes, we show that DNA damage signaling triggers a chronic autoinflammatory response leading to fat depletion. Ercc1-/- and aP2-Ercc1F/- fat depots show extensive gene expression similarities to lipodystrophic Pparγ(ldi/+) animals, focal areas of ruptured basement membrane, the reappearance of primary cilia, necrosis, fibrosis, and a marked decrease in adiposity. We find that persistent DNA damage in aP2-Ercc1F/- fat depots and in adipocytes ex vivo triggers the induction of proinflammatory factors by promoting transcriptionally active histone marks and the dissociation of nuclear receptor corepressor complexes from promoters; the response is cell autonomous and requires ataxia telangiectasia mutated (ATM). Thus, persistent DNA damage-driven autoinflammation plays a causative role in adipose tissue degeneration, with important ramifications for progressive lipodystrophies and natural aging.

Indexed as

DNA DamageAdipocytesAdipose TissueAnimalsAtaxia Telangiectasia Mutated ProteinsCells, CulturedCytokinesDNA-Binding ProteinsDNA RepairEndonucleasesFanconi Anemia Complementation Group ProteinsFatty Acid-Binding ProteinsHistonesMiceMice, KnockoutPPAR gammaAtaxia Telangiectasia Mutated ProteinsCytokinesDNA-Binding ProteinsEndonucleasesErcc1 protein, mouseFabp4 protein, mouseFANCI protein, mouseFanconi Anemia Complementation Group ProteinsFatty Acid-Binding ProteinsHistonesPPAR gammaRad51 Recombinase

Identifiers

PMID24011075
PMCPMC4116679
OpenAlexW2078519775

What OpenQuestion holds

Textmetadata
LicenceTDM
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.