Evidence map›Paper›PMID 39095660›Full record

ReviewSeminars in immunopathology2024

Crosstalk between the DNA damage response and cellular senescence drives aging and age-related diseases.

Ajmal Ahmad, Anneliesse Braden, Sazzad Khan, Jianfeng Xiao, Mohammad Moshahid Khan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
  2. Sanguinarine chloride exerts its antitumor effects on enzalutamide-resistant prostate cancer by inhibiting cell proliferation and promoting senescence via targeting AR signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  3. LiposomalInternational journal of molecular sciences · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025
    Review
  12. Article
  13. From Genome to Geroscience: How DNA Damage Shapes Systemic Decline.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  14. Review
  15. Article
  16. Djulis (Molecules (Basel, Switzerland) · 2025
    Review
  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

5 authors.

Ajmal AhmadDepartment of Ophthalmology, College of Medicine, King Saud University Riyadh, Riyadh, Saudi Arabia.
Anneliesse BradenDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Suite 415 Link Building, Memphis, TN, 38163, USA.
Sazzad KhanDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Suite 415 Link Building, Memphis, TN, 38163, USA.
Jianfeng XiaoDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Suite 415 Link Building, Memphis, TN, 38163, USA.
Mohammad Moshahid KhanDepartment of Neurology, College of Medicine, University of Tennessee Health Science Center, 855 Monroe Avenue, Suite 415 Link Building, Memphis, TN, 38163, USA. mkhan26@uthsc.edu.ORCID http://orcid.org/0000-0003-4679-294X

Funding

Novel DNA damage-Based Mechanisms and Therapeutics for Parkinson’s diseaseR21NS128519 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHAN, MOHAMMAD MOSHAHID · 2022 to 2022
$424k
Development of a novel gene therapy for the treatment of tauopathyR03AG075597 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KHAN, MOHAMMAD MOSHAHID, POURMOTABBED, TAYEBEH · 2022 to 2022
$308k
NIH HHS R03AG075597NIH HHS R21NS128519NINDS NIH HHS R21 NS128519
6 · The paper itself

Abstract

Cellular senescence is a crucial process of irreversible cell-cycle arrest, in which cells remain alive, but permanently unable to proliferate in response to distinct types of stressors. Accumulating evidence suggests that DNA damage builds over time and triggers DNA damage response signaling, leading to cellular senescence. Cellular senescence serves as a platform for the perpetuation of inflammatory responses and is central to numerous age-related diseases. Defects in DNA repair genes or senescence can cause premature aging disease. Therapeutic approaches limiting DNA damage or senescence contribute to a rescued phenotype of longevity and neuroprotection, thus suggesting a mechanistic interaction between DNA damage and senescence. Here, we offer a unique perspective on the crosstalk between the DNA damage response pathway and senescence as well as their contribution to age-related diseases. We further summarize recent progress on the mechanisms and therapeutics of senescence, address existing challenges, and offering new insights and future directions in the senescence field.

Indexed as

AgingCellular SenescenceDNA DamageDNA RepairSignal TransductionAnimalsDisease SusceptibilityHumansAgingAlzheimer’s diseaseAnti-senescence therapyDNA damageInflammationNeurodegenerationSenescence

Identifiers

What OpenQuestion holds

Textmetadata
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.