Evidence map›Paper›PMID 26761790›Full record

ArticlePloS one2016

Endothelial Dysfunction in Rheumatoid Arthritis: Mechanistic Insights and Correlation with Circulating Markers of Systemic Inflammation.

Perle Totoson, Katy Maguin-Gaté, Maude Nappey, Daniel Wendling, Céline Demougeot

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Adjuvant-induced arthritis promotes vascular hyporesponsiveness to phenylephrine through a nitric oxide-related mechanism.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Repercussions of adjuvant-induced arthritis on body composition, soleus muscle, and heart muscle of rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Perle TotosonEA 4267 FDE, FHU INCREASE, Univ. Bourgogne Franche-Comté, Besançon, France.
Katy Maguin-GatéEA 4267 FDE, FHU INCREASE, Univ. Bourgogne Franche-Comté, Besançon, France.
Maude NappeyEA 4267 FDE, FHU INCREASE, Univ. Bourgogne Franche-Comté, Besançon, France.
Daniel WendlingService de Rhumatologie, CHRU Besançon, Besançon, France.
Céline DemougeotEA 4267 FDE, FHU INCREASE, Univ. Bourgogne Franche-Comté, Besançon, France.
Université Bourgogne Franche-Comté · FRCentre Hospitalier Universitaire de Besançon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo determine mechanisms involved in endothelial dysfunction (ED) during the course of arthritis and to investigate the link between cytokines, chemokines and osteoprotegerin. APPROACH AND

resultsExperiments were conducted on aortic rings at day 4 (preclinical), day 11 (onset of disease), day 33 (acute disease) and day 90 (chronic disease) after adjuvant-induced arthritis (AIA) in Lewis rats. At day 4, the unique vascular abnormality was a reduced norepinephrine-induced constriction. At day 11, endothelial function assessed by the relaxation to acetylcholine was normal despite increased cyclo-oxygenase-2 activity (COX-2) and overproduction of superoxide anions that was compensated by increased nitric oxide synthase (NOS) activity. At day 33, ED apparition coincides with the normalization of NOS activity. At day 90, ED was only observed in rats with a persisting imbalance between endothelial NOS and COX-2 pathways and higher plasma levels of IL-1β and TNFα. Plasma levels of IL-1β, TNFα and MIP-1α negatively correlated with Ach-induced relaxation throughout the course of AIA.

conclusionsOur data identified increased endothelial NOS activity as an important compensatory response that opposes the ED in the early arthritis. Thereafter, a cross-talk between endothelial COX-2/NOS pathways appears as an important element for the occurrence of ED. Our results encourage determining the clinical value of IL-1β, TNFα and MIP-1α as biomarkers of ED in RA.

Indexed as

AcetylcholineAnimalsArthritis, ExperimentalArthritis, RheumatoidBiomarkersChemokinesCyclic N-OxidesCyclooxygenase 2Disease ProgressionEndothelium, VascularImmunizationInflammationMaleNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIINitrobenzenesAcetylcholineBiomarkersChemokinesCyclic N-OxidesCyclooxygenase 2N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIINitrobenzenesNitroprussideOsteoprotegerinSpin LabelsSulfonamidesSuperoxidestempol

Identifiers

PMID26761790
PMCPMC4711944
OpenAlexW2232733718

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.