Evidence map›Paper›PMID 28985345›Full record

ArticleNucleic acids research2017

Replication stress-induced endogenous DNA damage drives cellular senescence induced by a sub-lethal oxidative stress.

Gireedhar Venkatachalam, Uttam Surana, Marie-Véronique Clément

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.0field-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

51 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Functional Characterization ofFoods (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Inflammation and DNA damage: cause, effect or both.Nature reviews. Rheumatology · 2023
    Review
  18. Article
  19. The Telomere-Telomerase System Is Detrimental to Health at High-Altitude.International journal of environmental research and public health · 2023
    Article
  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

3 authors at 3 institutions in 1 country.

Gireedhar VenkatachalamDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117596, Singapore.
Uttam SuranaInstitute of Molecular and Cell Biology, Agency for Science Technology and Research, Proteos, Singapore 138673, Singapore.
Marie-Véronique ClémentDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117596, Singapore.
Agency for Science, Technology and Research · SGBioprocessing Technology Institute · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although oxidative stress has been shown to induce senescence and replication stress independently, no study has implicated unresolved replication stress as the driver for cellular senescence in response to oxidative stress. Using cells exposed to increasing concentrations of hydrogen peroxide, we show that sub-lethal amount of exogenous hydrogen peroxide induces two waves of DNA damage. The first wave is rapid and transient while the second wave coincides with the cells transition from the S to the G2/M phases of cell cycle. Subsequently, cells enter growth arrest accompanied by the acquisition of senescence-associated characteristics. Furthermore, a p53-dependent decrease in Rad51, which is associated with the formation of DNA segments with chromatin alterations reinforcing senescence, and Lamin B1 that is involved in chromatin remodeling, is observed during the establishment of the senescent phenotype. On the other hand, increase in senescence associated-β-Gal activity, a classical marker of senescence and HMGA2, a marker of the senescence-associated heterochromatin foci, is shown to be independent of p53. Together, our findings implicate replication stress-induced endogenous DNA damage as the driver for the establishment of cellular senescence upon sub-lethal oxidative stress, and implicate the role of p53 in some but not all hallmarks of the senescent phenotype.

Indexed as

DNA DamageDNA ReplicationAnimalsCell LineCellular SenescenceDNA Breaks, Double-StrandedDNA Breaks, Single-StrandedHistonesHMGA2 ProteinLamin Type BMicronuclei, Chromosome-DefectiveOxidative StressRad51 RecombinaseRatsTumor Suppressor Protein p53HistonesHMGA2 ProteinLamin Type BRad51 RecombinaseTumor Suppressor Protein p53

Identifiers

PMID28985345
PMCPMC5737622
OpenAlexW2742001951

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.