Evidence map›Paper›PMID 33208917›Full record

ReviewNature reviews. Rheumatology2021

Mechanisms and therapeutic implications of cellular senescence in osteoarthritis.

Philip R Coryell, Brian O Diekman, Richard F Loeser

Registry-linked trialOpen access · greenAbstract readComparative StudyReview
In one paragraph

Review in Nature reviews. Rheumatology, 2021. 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 442 papers.

0numbers the graph read from it
0cells of the map it votes in
442citing papers in PubMed
53.0field-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

442 citing papers in PubMed, 715 citations in OpenAlex.

  1. Trial
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  4. Review
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  6. Review
  7. Emerging therapies for knee osteoarthritis.Nature reviews. Rheumatology · 2026
    Review
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  12. Review
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  20. Review

382 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.

Philip R CoryellDivision of Rheumatology, Allergy, and Immunology, Thurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Brian O DiekmanDivision of Rheumatology, Allergy, and Immunology, Thurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA.
Richard F LoeserDivision of Rheumatology, Allergy, and Immunology, Thurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA. richard_loeser@med.unc.edu.ORCID 0000-0003-2832-6144
University of North Carolina at Chapel Hill · US

Funding

Oxidative Stress and the Development of OsteoarthritisR01AG044034 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICHARD F LOESER · 2012 to 2026
$5.7M
Integrin Function in CartilageR37AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2012 to 2021
$4.1M
NIAMS NIH HHS R37 AR049003NIA NIH HHS R01 AG044034
6 · The paper itself

Abstract

The development of osteoarthritis (OA) correlates with a rise in the number of senescent cells in joint tissues, and the senescence-associated secretory phenotype (SASP) has been implicated in cartilage degradation and OA. Age-related mitochondrial dysfunction and associated oxidative stress might induce senescence in joint tissue cells. However, senescence is not the only driver of OA, and the mechanisms by which senescent cells contribute to disease progression are not fully understood. Furthermore, it remains uncertain which joint cells and SASP-factors contribute to the OA phenotype. Research in the field has looked at developing therapeutics (namely senolytics and senomorphics) that eliminate or alter senescent cells to stop disease progression and pathogenesis. A better understanding of how senescence contributes to joint dysfunction may enhance the effectiveness of these approaches and provide relief for patients with OA.

Indexed as

AgeismAgingAnimalsAntibodies, Monoclonal, HumanizedBiomarkersCartilage, ArticularCellular SenescenceChondrocytesClinical Trials as TopicDisease ProgressionDNA DamageHumansHypolipidemic AgentsMiceModels, AnimalOsteoarthritisAntibodies, Monoclonal, HumanizedBiomarkersHypolipidemic AgentsMTOR protein, humanProtein Kinase InhibitorsTOR Serine-Threonine Kinases

Identifiers

PMID33208917
PMCPMC8035495
OpenAlexW3101423962

What OpenQuestion holds

Textmetadata
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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.