Evidence map›Paper›PMID 23852002›Full record

ArticleAging2013

Identification of microRNAs dysregulated in cellular senescence driven by endogenous genotoxic stress.

Lolita S Nidadavolu, Laura J Niedernhofer, Saleem A Khan

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

  1. Identification of Oncogene-Induced Senescence-Associated MicroRNAs.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  2. Review
  3. Hypertrophic cardiomyopathy inThe journal of cardiovascular aging · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. MicroRNAs and the metabolic hallmarks of aging.Molecular and cellular endocrinology · 2017
    Review
  15. Review
  16. Review
  17. MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence.Oxidative medicine and cellular longevity · 2017
    Review
  18. Article
  19. Article
  20. Review
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

3 authors at 2 institutions in 1 country.

Lolita S NidadavoluDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA.
Laura J Niedernhofer
Saleem A Khan
University of Pittsburgh · USScripps Institution of Oceanography · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Pitt Integrated Clinical and Geroscience Research Training ProgramT32AG021885 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Aditi U Gurkar · 2003 to 2026
$6.7M
The contribution of DNA interstrand crosslinks to agingR01ES016114 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NIEDERNHOFER, LAURA JANE · 2007 to 2011
$2.5M
NCATS NIH HHS UL1 TR000005NIA NIH HHS T32 AG021885NIA NIH HHS T32AG021885NIEHS NIH HHS ES016114NIEHS NIH HHS R01 ES016114
6 · The paper itself

Abstract

XFE progeroid syndrome, a disease of accelerated aging caused by deficiency in the DNA repair endonuclease XPF-ERCC1, is modeled by Ercc1 knockout and hypomorphic mice. Tissues and primary cells from these mice senesce prematurely, offering a unique opportunity to identify factors that regulate senescence and aging. We compared microRNA (miRNA) expression in Ercc1-/- primary mouse embryonic fibroblasts (MEFs) and wild-type (WT) MEFs in different growth conditions to identify miRNAs that drive cellular senescence. Microarray analysis showed three differentially expressed miRNAs in passage 7 (P7) Ercc1-/- MEFs grown at 20% O2 compared to Ercc1-/- MEFs grown at 3% O2. Thirty-six differentially expressed miRNAs were identified in Ercc1-/- MEFs at P7 compared to early passage (P3) in 3% O2. Eight of these miRNAs (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b) were similarly downregulated in the liver of progeroid Ercc1-/Δ and old WT mice compared to adult WT mice, a tissue that senesces with aging. Three miRNAs (miR-449a, miR-455* and miR-128) were also downregulated in Ercc1-/Δ and WT old mice kidneys compared to young WT mice. We also discovered that the miRNA expression regulator Dicer is significantly downregulated in tissues of old mice and late passage cells compared to young controls. Collectively these results support the conclusion that the miRNAs identified may play an important role in staving off cellular senescence and their altered expression could be indicative of aging.

Indexed as

AnimalsCells, CulturedCellular SenescenceDNA-Binding ProteinsDNA DamageEndonucleasesFibroblastsGene Expression RegulationMiceMice, KnockoutMicroRNAsOligonucleotide Array Sequence AnalysisDNA-Binding ProteinsEndonucleasesErcc1 protein, mouseMicroRNAs

Identifiers

PMID23852002
PMCPMC3824412
OpenAlexW2150953255

What OpenQuestion holds

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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.