Evidence map›Paper›PMID 18346777›Full record

ReviewMechanisms of ageing and development

DNA double-strand breaks: a potential causative factor for mammalian aging?

Han Li, James R Mitchell, Paul Hasty

Open access · greenAbstract readReview
In one paragraph

Review in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Aging · 2022
    Article
  6. Article
  7. Review
  8. The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Do p53 stress responses impact organismal aging?Translational cancer research · 2016
    Article
  17. Article
  18. Inevitability and containment of replication errors for eukaryotic genome lengths spanning megabase to gigabase.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  19. DNA Damage in Chronic Kidney Disease: Evaluation of Clinical Biomarkers.Oxidative medicine and cellular longevity · 2016
    Review
  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 2 institutions in 2 countries.

Han LiDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center, 15355 Lambda Drive, San Antonio, TX 78245-3207, USA. hli@cnio.es
James R Mitchell
Paul Hasty
The University of Texas Health Science Center at San Antonio · USCancer Genomics Centre · NL

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
Models for DNA repair and cell cycle control variantsU01ES011044 · NIEHS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 2001 to 2006
$5.1M
XRCC5 MUTANT MICE AND CELL LINESR01CA076317 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI HASTY, EDWARD PAUL · 1997 to 2005
$1.0M
NCI NIH HHS R01 CA076317NCI NIH HHS R01 CA 76317-05A1NIA NIH HHS P01 AG017242NIA NIH HHS P01 AG 17242NIEHS NIH HHS U01 ES011044NIEHS NIH HHS U01 ES 11044
6 · The paper itself

Abstract

Aging is a pleiotropic and stochastic process influenced by both genetics and environment. As a result the fundamental underlying causes of aging are controversial and likely diverse. Genome maintenance and in particular the repair of DNA damage is critical to ensure longevity needed for reproduction and as a consequence imperfections or defects in maintaining the genome may contribute to aging. There are many forms of DNA damage with double-strand breaks (DSBs) being the most toxic. Here we discuss DNA DSBs as a potential causative factor for aging including factors that generate DNA DSBs, pathways that repair DNA DSBs, consequences of faulty or failed DSB repair and how these consequences may lead to age-dependent decline in fitness. At the end we compare mouse models of premature aging that are defective for repairing either DSBs or UV light-induced lesions. Based on these comparisons we believe the basic mechanisms responsible for their aging phenotypes are fundamentally different demonstrating the complex and pleiotropic nature of this process.

Indexed as

DNA Breaks, Double-StrandedAgingAging, PrematureAnimalsDNA RepairHumansMammalsMiceMutation

Identifiers

PMID18346777
PMCPMC2517577
OpenAlexW2091060354

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.