Evidence map›Paper›PMID 30944259›Full record

ArticleJCI insight2019

Senescence cell-associated extracellular vesicles serve as osteoarthritis disease and therapeutic markers.

Ok Hee Jeon, David R Wilson, Cristina C Clement, Sona Rathod, Christopher Cherry, Bonita Powell, Zhenghong Lee, Ahmad M Khalil, Jordan J Green, Judith Campisi and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 2% 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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. From pathogenesis to therapy: extracellular vesicles in osteoarthritis.Frontiers in bioengineering and biotechnology · 2026
    Review
  18. Review
  19. Review
  20. Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025
    Review

53 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

13 authors at 5 institutions in 1 country.

Ok Hee JeonBuck Institute for Research on Aging, Novato, California, USA.
David R WilsonTranslational Tissue Engineering Center, Wilmer Eye Institute, and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Cristina C ClementDepartment of Pathology, Orthopedic Surgery, Microbiology and Immunology, Albert Einstein College of Medicine, New York, New York, USA.
Sona RathodTranslational Tissue Engineering Center, Wilmer Eye Institute, and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Christopher CherryTranslational Tissue Engineering Center, Wilmer Eye Institute, and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Bonita PowellDepartment of Molecular and Comparative Pathobiology and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Zhenghong LeeDepartment of Radiology, Case Western Reserve University, University Hospitals Bolwell, Cleveland, Ohio, USA.
Ahmad M KhalilGenetics and Genome Sciences and Center for Multimodal Evaluation of Engineered Cartilage, Case Western Reserve University, Cleveland, Ohio, USA.
Jordan J GreenTranslational Tissue Engineering Center, Wilmer Eye Institute, and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Judith CampisiBuck Institute for Research on Aging, Novato, California, USA.
Laura SantambrogioDepartment of Pathology, Orthopedic Surgery, Microbiology and Immunology, Albert Einstein College of Medicine, New York, New York, USA.
Kenneth W WitwerDepartment of Molecular and Comparative Pathobiology and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jennifer H ElisseeffTranslational Tissue Engineering Center, Wilmer Eye Institute, and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Johns Hopkins University · USAlbert Einstein College of Medicine · USBuck Institute for Research on Aging · USCase Western Reserve University · USUniversity Hospitals of Cleveland · US

Funding

TR&D-4: Growing Tissue in the Scalable, Modular, Automated, and Closed (SMAC) FoundryP41EB021911 · NIBIB · CASE WESTERN RESERVE UNIVERSITY · PI HARIHARA BASKARAN · 2016 to 2026
$13.9M
CELLULAR SENESCENCE AND CONTROL OF GENE EXPRESSIONR37AG009909 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI CAMPISI, JUDITH · 1995 to 2015
$7.6M
DYNAMICS AND TUNING OF THE MHC II PRESENTED PEPTIDOMER01AI137198 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SANTAMBROGIO, LAURA, STERN, LAWRENCE J. · 2018 to 2022
$4.6M
Effects of Glycation and Carbonylation on MHC II-restricted immunityR01AI146180 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SANTAMBROGIO, LAURA, STERN, LAWRENCE J. · 2020 to 2024
$3.7M
MHC class II-restricted immune response in immunosenescenceR01AG045223 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI SANTAMBROGIO, LAURA · 2014 to 2018
$1.7M
Cellular senescence and control of gene expressionR56AG009909 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2017 to 2017
$592k
NIAID NIH HHS R01 AI137198NIAID NIH HHS R01 AI146180NIA NIH HHS R01 AG045223NIA NIH HHS R37 AG009909NIA NIH HHS R56 AG009909NIBIB NIH HHS P41 EB021911
6 · The paper itself

Abstract

Senescent cells (SnCs) are increasingly recognized as central effector cells in age-related pathologies. Extracellular vesicles (EVs) are potential cellular communication tools through which SnCs exert central effector functions in the local tissue environment. To test this hypothesis in a medical indication that could be validated clinically, we evaluated EV production from SnCs enriched from chondrocytes isolated from human arthritic cartilage. EV production increased in a dose-responsive manner as the concentration of SnCs increased. The EVs were capable of transferring senescence to nonsenescent chondrocytes and inhibited cartilage formation by non-SnCs. microRNA (miR) profiles of EVs isolated from human arthritic synovial fluid did not fully overlap with the senescent chondrocyte EV profiles. The effect of SnC clearance was tested in a murine model of posttraumatic osteoarthritis. miR and protein profiles changed after senolytic treatment but varied depending on age. In young animals, senolytic treatment altered expression of miR-34a, -30c, -125a, -24, -92a, -150, and -186, and this expression correlated with cartilage production. The primary changes in EV contents in aged mice after senolytic treatment, which only reduced pain and degeneration, were immune related. In sum, EV contents found in synovial fluid may serve as a diagnostic for arthritic disease and indicator for therapeutic efficacy of senolytic treatment.

Indexed as

AgedAged, 80 and overAnimalsArthroplasty, Replacement, KneeBiomarkersCartilage, ArticularCells, CulturedCellular SenescenceChondrocytesDisease Models, AnimalDrug MonitoringExtracellular VesiclesHumansMaleMiceMicroRNAsBiomarkersMicroRNAsAgingCartilageOsteoarthritisTherapeutics

Identifiers

PMID30944259
PMCPMC6483636
OpenAlexW2930088324

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.