Evidence map›Paper›PMID 23448364›Full record

ArticleAging cell2013

Oxidative stress activates a specific p53 transcriptional response that regulates cellular senescence and aging.

Valentina Gambino, Giulia De Michele, Oriella Venezia, Pierluigi Migliaccio, Valentina Dall'Olio, Loris Bernard, Simone Paolo Minardi, Maria Agnese Della Fazia, Daniela Bartoli, Giuseppe Servillo and 6 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Aging cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 3 pooled it
6.5field-weighted citation impact, top 3% 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

80 citing papers in PubMed, 3 syntheses or guidelines pooled it, 151 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  10. Effect of physical activity in lymphocytes senescence burden in patients with COPD.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  17. Article
  18. JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023
    Review
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 2 countries.

Valentina GambinoEuropean Institute of Oncology, Via Ripamonti 435, Milan, 20141, Italy.
Giulia De Michele
Oriella Venezia
Pierluigi Migliaccio
Valentina Dall'Olio
Loris Bernard
Simone Paolo Minardi
Maria Agnese Della Fazia
Daniela Bartoli
Giuseppe Servillo
Myriam Alcalay
Lucilla Luzi
Marco Giorgio
Heidi Scrable
Pier Giuseppe Pelicci
Enrica Migliaccio
Ripamonti · ITIFOM · ITUniversity of Perugia · ITUniversity of Milan · ITUniversity of Massachusetts Chan Medical School · USUniversity of Siena · IT

Funding

TRANSLOCATION OF p66Shc: KINETICS, FUNCTION, APOPTOSISP01AG025532 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KIM, KYOUNGMI · 2007 to 2017
$12.1M
NIA NIH HHS 1P01AG025532-01A1NIA NIH HHS P01 AG025532
6 · The paper itself

Abstract

Oxidative stress is a determining factor of cellular senescence and aging and a potent inducer of the tumour-suppressor p53. Resistance to oxidative stress correlates with delayed aging in mammals, in the absence of accelerated tumorigenesis, suggesting inactivation of selected p53-downstream pathways. We investigated p53 regulation in mice carrying deletion of p66, a mutation that retards aging and confers cellular resistance and systemic resistance to oxidative stress. We identified a transcriptional network of ~200 genes that are repressed by p53 and encode for determinants of progression through mitosis or suppression of senescence. They are selectively down-regulated in cultured fibroblasts after oxidative stress, and, in vivo, in proliferating tissues and during physiological aging. Selectivity is imposed by p66 expression and activation of p44/p53 (also named Delta40p53), a p53 isoform that accelerates aging and prevents mitosis after protein damage. p66 deletion retards aging and increases longevity of p44/p53 transgenic mice. Thus, oxidative stress activates a specific p53 transcriptional response, mediated by p44/p53 and p66, which regulates cellular senescence and aging.

Indexed as

AnimalsCell CycleCells, CulturedCellular SenescenceHepatocytesLongevityMiceMice, KnockoutOxidative StressPeptide FragmentsProtein IsoformsShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Thymus GlandTranscription FactorsTranscription, GeneticPeptide FragmentsProtein IsoformsShc1 protein, mouseShc Signaling Adaptor ProteinsSrc Homology 2 Domain-Containing, Transforming Protein 1Transcription FactorsTumor Suppressor Protein p53WDR77 protein, mouse

Identifiers

PMID23448364
PMCPMC3709138
OpenAlexW1965718763

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.