Evidence map›Paper›PMID 18160407›Full record

ReviewNucleic acids research2007

The role of DNA damage repair in aging of adult stem cells.

Jonathan Kenyon, Stanton L Gerson

Open access · goldAbstract readReview
In one paragraph

Review in Nucleic acids research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Stem Cell Aging and Regenerative Medicine.Advances in experimental medicine and biology · 2021
    Review
  14. Review
  15. Osteocyte Cellular Senescence.Current osteoporosis reports · 2020
    Review
  16. A Preliminary Study: Human Fibroid Stro-1Reproductive sciences (Thousand Oaks, Calif.) · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Identification of Senescent Cells in the Bone Microenvironment.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Article

2 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

2 authors at 1 institution in 1 country.

Jonathan KenyonCase Western Reserve University and the Ireland Cancer Center, University Hospitals Case Medical Center, Cleveland, OH 44106, USA.
Stanton L Gerson
University Hospitals Case Medical Center · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
Declining DNA repair in Aging Hematopoietic Stem CellR01AG024916 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI GERSON, STANTON L. · 2004 to 2008
$1.6M
NCI NIH HHS P30 CA043703NCI NIH HHS P30 CA043703-18NIA NIH HHS R01 AG024916NIA NIH HHS R01 AG024916-03
6 · The paper itself

Abstract

DNA repair maintains genomic stability and the loss of DNA repair capacity results in genetic instability that may lead to a decline of cellular function. Adult stem cells are extremely important in the long-term maintenance of tissues throughout life. They regenerate and renew tissues in response to damage and replace senescent terminally differentiated cells that no longer function. Oxidative stress, toxic byproducts, reduced mitochondrial function and external exposures all damage DNA through base modification or mis-incorporation and result in DNA damage. As in most cells, this damage may limit the survival of the stem cell population affecting tissue regeneration and even longevity. This review examines the hypothesis that an age-related loss of DNA damage repair pathways poses a significant threat to stem cell survival and longevity. Normal stem cells appear to have strict control of gene expression and DNA replication whereas stem cells with loss of DNA repair may have altered patterns of proliferation, quiescence and differentiation. Furthermore, stem cells with loss of DNA repair may be susceptible to malignant transformation either directly or through the emergence of cancer-prone stem cells. Human diseases and animal models of loss of DNA repair provide longitudinal analysis of DNA repair processes in stem cell populations and may provide links to the physiology of aging.

Indexed as

Cellular SenescenceDNA RepairAdultAging, PrematureAnimalsDNA-Binding ProteinsDNA DamageDNA Mismatch RepairHumansMiceNeoplastic Stem CellsRecQ HelicasesStem CellsTelomeraseDNA-Binding ProteinsRecQ HelicasesTelomerase

Identifiers

PMID18160407
PMCPMC2190724
OpenAlexW2163352078

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.