Evidence map›Paper›PMID 12651622›Full record

ArticleThe American journal of pathology2003

Telomere shortening and cellular senescence in a model of chronic renal allograft rejection.

Simone A Joosten, Vanessa van Ham, Claire E Nolan, Maria C Borrias, Alan G Jardine, Paul G Shiels, Cees van Kooten, Leendert C Paul

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. P16INK4A-More Than a Senescence Marker.Life (Basel, Switzerland) · 2022
    Review
  7. Article
  8. Telomere shortening in patients on long-term hemodialysis.Chronic diseases and translational medicine · 2021
    Article
  9. Review
  10. Review
  11. Cellular Senescence: A New Player in Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2020
    Review
  12. The emerging role of cellular senescence in renal diseases.Journal of cellular and molecular medicine · 2020
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Joint Assessment of Donor and Recipient hTERT Gene Polymorphism Provides Additional Information for Early Kidney Transplantation Outcomes.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  19. Cellular senescence in renal ageing and disease.Nature reviews. Nephrology · 2017
    Review
  20. Telomere Length Assessment for Prediction of Organ Transplantation Outcome. Future or Failure: A Review of the Literature.Medical science monitor : international medical journal of experimental and clinical research · 2017
    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

8 authors at 2 institutions in 2 countries.

Simone A JoostenDepartment of Nephrology, Leiden University Medical Center, Leiden, The Netherlands. S.A.Joosten@LUMC.nl
Vanessa van Ham
Claire E Nolan
Maria C Borrias
Alan G Jardine
Paul G Shiels
Cees van Kooten
Leendert C Paul
Leiden University Medical Center · NLUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence has been suggested to play a role in the deterioration of renal graft function and has been linked to telomere shortening. We have investigated markers of cellular senescence in the F344 to LEW rat model of chronic renal transplant rejection. Syngeneic and LEW to F344 transplants were used as controls. Substantial telomere shortening was observed in all transplants, including allogeneic and syngeneic grafts from day 7 post-transplant onwards. Ischemia of native F344 kidneys was already sufficient to induce telomere shortening. It is known that shortened telomeres can activate cell cycle regulators, such as p21 and p16. Accordingly, all cases showed a transient p21 increase, with a maximum at day 7 and a sustained expression of p16. Importantly, senescence-associated beta-galactosidase staining, a cytological marker for senescence, was only observed in tubular epithelial cells of chronically rejecting F344 allografts from day 30 post-transplantation onwards. Long-term surviving LEW allografts or syngeneic F344 grafts were negative for senescence-associated beta-galactosidase. In conclusion, ischemia during transplantation results in telomere shortening and subsequent activation of p21 and p16, whereas senescence-associated beta-galactosidase staining is only present in chronically rejecting kidney grafts.

Indexed as

AnimalsCell CycleCellular SenescenceChronic DiseaseDisease Models, AnimalGraft RejectionIschemiaKidneyKidney TransplantationMaleRatsRats, Inbred F344Rats, Inbred LewReperfusionTelomereTransplantation, Homologous

Identifiers

PMID12651622
PMCPMC1851231
OpenAlexW2008160502

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.