Evidence map›Paper›PMID 32164429›Full record

ReviewAntioxidants & redox signaling2021

Senescence in Post-Mitotic Cells: A Driver of Aging?

Thomas von Zglinicki, Tengfei Wan, Satomi Miwa

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
–field-weighted citation impact
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

87 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026
    Review
  5. Senescent-Like Myofibers Contribute to Anti-Regenerative Cytokine Signaling in Duchenne Muscular Dystrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. IFN-Mediated Bronchial Epithelium Cellular Senescence in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024
    Review
  20. BRCA1 Promotes Repair of DNA Damage in Cochlear Hair Cells and Prevents Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article

27 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

3 authors.

Thomas von ZglinickiAgeing Research Laboratories, Faculty of Medical Sciences, Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom.
Tengfei WanAgeing Research Laboratories, Faculty of Medical Sciences, Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom.
Satomi MiwaAgeing Research Laboratories, Faculty of Medical Sciences, Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom.

Funding

Biotechnology and Biological Sciences Research Council BB/S006710/1Cancer Research UK C12161/A24009Medical Research Council MR/P020941/1
6 · The paper itself

Abstract

PubMed holds no abstract for this paper.

Indexed as

Resting Phase, Cell CycleAgingAnimalsAutophagyBiomarkersCellular SenescenceHumansMitochondriaMitophagyNeuronsOrgan SpecificityOsteocytesBiomarkersagingpost-mitoticsenescence

Identifiers

PMID32164429
PMCPMC7821432

What Socratic 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 Socratic graph.