Evidence map›Paper›PMID 28124466›Full record

ReviewAging cell2017

Cellular senescence in osteoarthritis pathology.

Kendal McCulloch, Gary J Litherland, Taranjit Singh Rai

Registry-linked trialOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05637216 (A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients), which is not on this map. Cited by 218 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 6 pooled it
20.8field-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.

NCT05637216 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients

TypeinterventionalSponsorShaw Cancer CenterRan2023 to 2027Enrolled43ConditionsRadiation Induced FibrosisArmsLosartan 25 milligram capsule, Placebo
3 · Its place in the literature

Who cites it

218 citing papers in PubMed, 6 syntheses or guidelines pooled it, 361 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

158 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

3 authors at 1 institution in 1 country.

Kendal McCullochInstitute of Biomedical and Environmental Health Research, University of the West of Scotland, Paisley, PA1 2BE, UK.
Gary J LitherlandInstitute of Biomedical and Environmental Health Research, University of the West of Scotland, Paisley, PA1 2BE, UK.
Taranjit Singh RaiInstitute of Biomedical and Environmental Health Research, University of the West of Scotland, Paisley, PA1 2BE, UK.ORCID 0000-0002-7276-7492
University of the West of Scotland · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a state of stable proliferation arrest of cells. The senescence pathway has many beneficial effects and is seen to be activated in damaged/stressed cells, as well as during embryonic development and wound healing. However, the persistence and accumulation of senescent cells in various tissues can also impair function and have been implicated in the pathogenesis of many age-related diseases. Osteoarthritis (OA), a severely debilitating chronic condition characterized by progressive tissue remodeling and loss of joint function, is the most prevalent disease of the synovial joints, and increasing age is the primary OA risk factor. The profile of inflammatory and catabolic mediators present during the pathogenesis of OA is strikingly similar to the secretory profile observed in 'classical' senescent cells. During OA, chondrocytes (the sole cell type present within articular cartilage) exhibit increased levels of various senescence markers, such as senescence-associated beta-galactosidase (SAβGal) activity, telomere attrition, and accumulation of p16ink4a. This suggests the hypothesis that senescence of cells within joint tissues may play a pathological role in the causation of OA. In this review, we discuss the mechanisms by which senescent cells may predispose synovial joints to the development and/or progression of OA, as well as touching upon various epigenetic alterations associated with both OA and senescence.

Indexed as

Cellular SenescenceAnimalsEpigenesis, GeneticHumansModels, BiologicalOsteoarthritiscellular senescenceepigeneticsosteoarthritis

Identifiers

PMID28124466
PMCPMC5334539
OpenAlexW2582214777

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.