Evidence map›Paper›PMID 26571131›Full record

ArticlePloS one2015

Protective Role of the Interleukin 33 rs3939286 Gene Polymorphism in the Development of Subclinical Atherosclerosis in Rheumatoid Arthritis Patients.

Raquel López-Mejías, Fernanda Genre, Sara Remuzgo-Martínez, Montserrat Robustillo-Villarino, Mercedes García-Bermúdez, Javier Llorca, Alfonso Corrales, Carlos González-Juanatey, Begoña Ubilla, José A Miranda-Filloy and 13 more

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. The Influence of Genetic Polymorphisms ofInternational journal of dentistry · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022
    Review
  7. Article
  8. IL-33/IL-31 Axis in Osteoporosis.International journal of molecular sciences · 2020
    Review
  9. Atherosclerosis in Rheumatoid Arthritis: Promoters and Opponents.Clinical reviews in allergy & immunology · 2020
    Review
  10. Article
  11. Article
  12. Mechanisms of vascular comorbidity in autoimmune diseases.Current opinion in rheumatology · 2018
    Review
  13. Article
  14. Article
  15. Article
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

23 authors.

Raquel López-MejíasEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Fernanda GenreEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Sara Remuzgo-MartínezEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Montserrat Robustillo-VillarinoRheumatology Department, Hospital Universitario Doctor Peset, Valencia, Spain.
Mercedes García-BermúdezInstitute of Parasitology and Biomedicine López-Neyra, IPBLN-CSIC, Granada, Spain.
Javier LlorcaDepartment of Epidemiology and Computational Biology, School of Medicine, University of Cantabria, and CIBER Epidemiología y Salud Pública (CIBERESP), IDIVAL, Santander, Spain.
Alfonso CorralesEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Carlos González-JuanateyCardiology Department, Hospital Lucus Augusti, Lugo, Spain.
Begoña UbillaEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
José A Miranda-FilloyRheumatology Department, Hospital Lucus Augusti, Lugo, Spain.
Verónica MijaresEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Trinitario PinaEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Ricardo BlancoEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.
Juan J Alegre-SanchoRheumatology Department, Hospital Universitario Doctor Peset, Valencia, Spain.
Marco A Ramírez HuarangaRheumatology Department, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain.
María D Mínguez SánchezRheumatology Department, Hospital General Universitario de Ciudad Real, Ciudad Real, Spain.
Beatriz Tejera SeguraRheumatology Department, Hospital Universitario de Canarias, Tenerife, Spain.
Iván Ferraz-AmaroRheumatology Department, Hospital Universitario de Canarias, Tenerife, Spain.
Esther VicenteRheumatology Department, Hospital Universitario la Princesa, IIS-Princesa, Madrid, Spain.
F David CarmonaInstitute of Parasitology and Biomedicine López-Neyra, IPBLN-CSIC, Granada, Spain.
Santos CastañedaRheumatology Department, Hospital Universitario la Princesa, IIS-Princesa, Madrid, Spain.
Javier MartínInstitute of Parasitology and Biomedicine López-Neyra, IPBLN-CSIC, Granada, Spain.
Miguel A González-GayEpidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo determine whether the interleukin-33 (IL-33)-interleukin-1 receptor like 1 (IL-1RL1) signaling pathway is implicated in the risk of subclinical atherosclerosis in patients with rheumatoid arthritis (RA).

methodsA total of 576 Spanish RA patients from Northern Spain were genotyped for 6 well-known IL33-IL1RL1 polymorphisms (IL33 rs3939286, IL33 rs7025417, IL33 rs7044343, IL1RL1 rs2058660, IL1RL1 rs2310173 and IL1RL1 rs13015714) by TaqMan genotyping assay. The presence of subclinical atherosclerosis was determined by the assessment of carotid intima-media thickness (cIMT) by carotid ultrasound (US).

resultsRA patients carrying the TT genotype of the IL33 rs3939286 polymorphism had lower cIMT values than those homozygous for the CC genotype (mean ± standard deviation (SD): 0.71 ± 0.14 mm versus 0.76 ± 0.16 mm, respectively) while patients carrying the CT genotype had intermediate cIMT values (mean ± SD: 0.73 ± 0.17 mm). Moreover, RA patients carrying the mutant allele T of the IL33 rs3939286 polymorphism exhibited significantly lower cIMT values than those carrying the wild allele C (mean ± SD: 0.72 ± 0.16 mm versus 0.75 ± 0.18 mm respectively; p = 0.04). The association of both genotype and allele frequencies of IL33 rs3939286 and cIMT levels remained statistically significant after adjustment for sex, age at the time of US study, follow-up and center (p = 0.006 and p = 0.0023, respectively), evidencing that the potential effect conferred by IL33 rs3939286 may be independent of confounder factors. No association with other IL33-IL1RL1 genetic variants was observed.

conclusionsIn conclusion, our results may suggest a potential protective effect of the IL33 rs3939286 allele T in the risk of subclinical atherosclerosis in patients with RA.

Indexed as

AdultAgedAllelesArthritis, RheumatoidAtherosclerosisCarotid ArteriesFemaleFollow-Up StudiesGene FrequencyGenotypeHumansInterleukin-33Linkage DisequilibriumMaleMiddle AgedPolymorphism, Single NucleotideIL1R1 protein, humanInterleukin-33Receptors, Interleukin-1 Type I

Identifiers

PMID26571131
PMCPMC4646618

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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.