Evidence map›Paper›PMID 32223966›Full record

ArticleInternational journal of cardiology2020

Circulating interleukins in relation to coronary artery disease, atrial fibrillation and ischemic stroke and its subtypes: A two-sample Mendelian randomization study.

Shuai Yuan, Ang Lin, Qi-Qiang He, Stephen Burgess, Susanna C Larsson

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

Article in International journal of cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
3.2field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Leveraging Mendelian randomization to inform drug discovery and development for ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 3 countries.

Shuai YuanUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden. Electronic address: shuai.yuan@ki.se.
Ang LinDepartment of Medicine Solna, Immunology and Allergy Unit, Karolinska Institutet, Stockholm, Sweden; Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden. Electronic address: ang.lin@ki.se.
Qi-Qiang HeSchool of Health Sciences, Wuhan University, Wuhan, China.
Stephen BurgessDepartment of Public Health and Primary Care, University of Cambridge, Cambridge, UK; MRC Biostatistics Unit, University of Cambridge, Cambridge, UK. Electronic address: sb452@medschl.cam.ac.uk.
Susanna C LarssonUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Surgical Sciences, Uppsala University, Uppsala, Sweden. Electronic address: susanna.larsson@ki.se.
Karolinska Institutet · SEMRC Biostatistics Unit · GBUppsala University · SEWuhan University · CN

Funding

Medical Research Council MC_UU_00002/7Wellcome Trust 204623Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

backgroundThe causal role of interleukins (ILs) for cardiovascular disease has not been fully elucidated. We conducted a Mendelian randomization study to investigate the associations of circulating ILs with coronary artery disease (CAD), atrial fibrillation (AF), and ischemic stroke. METHODS AND

resultsSingle-nucleotide polymorphisms associated with IL-1β, IL-1 receptor antagonist (IL-1ra), IL-2 receptor subunit alpha, IL-6, IL-16, IL-17 and IL-18 were identified from genome-wide association studies. Summary-level data of the outcomes were obtained from three large consortia. Genetic predisposition to higher IL-1ra levels were significantly associated with CAD. The odds ratio was 1.36 (95% confidence interval (CI), 1.14-1.63; P = 5.37 × 10

conclusionsThese results strengthen the evidence that IL-6 inhibition may offer a therapeutic approach for prevention of CAD, AF, and ischemic stroke. In contrast, IL-1 inhibition through raised IL-1ra levels may confer increased risk of CAD and cardioembolic stroke. The role of IL-16 for CAD warrants further investigation.

Indexed as

Atrial FibrillationBrain IschemiaCoronary Artery DiseaseIschemic StrokeStrokeGenome-Wide Association StudyHumansInterleukinsMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsInterleukinsAtrial fibrillationCoronary artery diseaseImmuneInterleukinsIschemic strokeMendelian randomization analysis

Identifiers

PMID32223966
PMCPMC7611848
OpenAlexW3012883283

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.