Evidence map›Paper›PMID 33166065›Full record

ReviewAging cell2020

On the evolution of cellular senescence.

Axel Kowald, João F Passos, Thomas B L Kirkwood

Open access · goldAbstract readReview
In one paragraph

Review in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
10.2field-weighted citation impact, top 1% 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

96 citing papers in PubMed, 181 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. p16 Beyond Senescence: Cancer Biology Lessons Applied to Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

36 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 at 3 institutions in 4 countries.

Axel KowaldCampus for Ageing and Vitality, Newcastle University Institute for Ageing, Newcastle upon Tyne, UK.ORCID 0000-0001-6448-4364
João F PassosDepartment of Physiology and Biomedical Engineering, Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
Thomas B L KirkwoodCampus for Ageing and Vitality, Newcastle University Institute for Ageing, Newcastle upon Tyne, UK.
Mayo Clinic in Florida · USNewcastle Hospitals - Campus for Ageing and Vitality · GBUniversity of Copenhagen · DK

Funding

US National Institutes of Health AG069048
6 · The paper itself

Abstract

The idea that senescent cells are causally involved in aging has gained strong support from findings that the removal of such cells alleviates many age-related diseases and extends the life span of mice. While efforts proceed to make therapeutic use of such discoveries, it is important to ask what evolutionary forces might have been behind the emergence of cellular senescence, in order better to understand the biology that we might seek to alter. Cellular senescence is often regarded as an anti-cancer mechanism, since it limits the division potential of cells. However, many studies have shown that senescent cells often also have carcinogenic properties. This is difficult to reconcile with the simple idea of an anti-cancer mechanism. Furthermore, other studies have shown that cellular senescence is involved in wound healing and tissue repair. Here, we bring these findings and ideas together and discuss the possibility that these functions might be the main reason for the evolution of cellular senescence. Furthermore, we discuss the idea that senescent cells might accumulate with age because the immune system had to strike a balance between false negatives (overlooking some senescent cells) and false positives (destroying healthy body cells).

Indexed as

Cellular SenescenceAgingAnimalsBiological EvolutionCarcinogenesisHumansLongevityMiceModels, BiologicalNeoplasmsWound Healingaginganti-agingcellular senescenceevolutionsenolytics

Identifiers

PMID33166065
PMCPMC7744960
OpenAlexW3099661466

What OpenQuestion 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 OpenQuestion graph.