Evidence map›Paper›PMID 38596783›Full record

ReviewFrontiers in aging2023

Senescence: A DNA damage response and its role in aging and Neurodegenerative Diseases.

Tejal Shreeya, Mohd Saifullah Ansari, Prabhat Kumar, Muskan Saifi, Ali A Shati, Mohammad Y Alfaifi, Serag Eldin I Elbehairi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
14.7field-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

39 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Journal of microbiology and biotechnology · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Frontiers in medicine · 2026
    Article
  17. Article
  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

7 authors at 4 institutions in 2 countries.

Tejal ShreeyaInstitute of Biophysics, Biological Research Center, Szeged, Hungary.
Mohd Saifullah AnsariInstitute of Genetics, Biological Research Center, Szeged, Hungary.
Prabhat KumarInstitute of Physiology, Medical School, University of Pécs, Pécs, Hungary.
Muskan SaifiS.S.V (PG) College, Hapur, Uttar Pradesh, India.
Ali A ShatiBiology Department, Faculty of Science, King Khalid University, Abha, Saudi Arabia.
Mohammad Y AlfaifiBiology Department, Faculty of Science, King Khalid University, Abha, Saudi Arabia.
Serag Eldin I ElbehairiBiology Department, Faculty of Science, King Khalid University, Abha, Saudi Arabia.
King Khalid University · SAInstitute of Biophysics · HUInstitute of Genetics · HUUniversity of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence is a complicated, multi-factorial, irreversible cell cycle halt that has a tumor-suppressing effect in addition to being a significant factor in aging and neurological diseases. Damaged DNA, neuroinflammation, oxidative stress and disrupted proteostasis are a few of the factors that cause senescence. Senescence is triggered by DNA damage which initiates DNA damage response. The DNA damage response, which includes the formation of DNA damage foci containing activated H2AX, which is a key factor in cellular senescence, is provoked by a double strand DNA break. Oxidative stress impairs cognition, inhibits neurogenesis, and has an accelerated aging effect. Senescent cells generate pro-inflammatory mediators known as senescence-associated secretory phenotype (SASP). These pro-inflammatory cytokines and chemokines have an impact on neuroinflammation, neuronal death, and cell proliferation. While it is tempting to think of neurodegenerative diseases as manifestations of accelerated aging and senescence, this review will present information on brain ageing and neurodegeneration as a result of senescence and DNA damage response.

Indexed as

DNA damage responseneurodegenerative diseasesneuroinflammationneuronal deathSASP and senescence

Identifiers

PMID38596783
PMCPMC11002673
OpenAlexW4393022698

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.