Evidence map›Paper›PMID 24903211›Full record

ArticleScientific reports2014

The roles of Ca2+/NFAT signaling genes in Kawasaki disease: single- and multiple-risk genetic variants.

Wei Wang, Jiao Lou, Rong Zhong, Yan-qi Qi, Na Shen, Xu-zai Lu, Yu-jia Wang, Qing Zhang, Li Zou, Jia-yu Duan and 3 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 3 pooled it
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 3 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Frontiers in immunology · 2023
    Article
  7. Immunogenetics of Kawasaki disease.Clinical reviews in allergy & immunology · 2020
    Review
  8. The role of CaScientific reports · 2020
    Article
  9. Article
  10. Review
  11. Kawasaki disease: etiopathogenesis and novel treatment strategies.Expert review of clinical immunology · 2017
    Review
  12. Review
  13. 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

13 authors at 3 institutions in 2 countries.

Wei Wang1] Children's Hospital, Zhejiang University School of Medicine, Hangzhou, PR China [2].
Jiao Lou1] Department of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China [2].
Rong ZhongDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Yan-qi QiChildren's Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
Na ShenDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Xu-zai LuGuangdong Women and Children Hospital, Guangzhou, PR China.
Yu-jia WangCentre Hospitalier de l'Université de Montréal, CRCHUM-Hôpital Notre-Dame, Pavillion DeSève, Montreal, Canada.
Qing ZhangChildren's Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
Li ZouDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Jia-yu DuanDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Jun-tao KeDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Xiao-ping MiaoDepartment of Epidemiology and Biostatistics and Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Fang-qi GongChildren's Hospital, Zhejiang University School of Medicine, Hangzhou, PR China.
Huazhong University of Science and Technology · CNCentre Hospitalier de l’Université de Montréal · CAGuangdong Province Women and Children Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca(2+)/nuclear factor of activated T-cells (Ca(2+)/NFAT) signaling pathway may play a crucial role in Kawasaki disease (KD). We investigated 16 genetic variants, selected by bioinformatics analyses or previous studies, in 7 key genes involved in this pathway in a Chinese population. We observed a significantly or marginally increased KD risk associated with rs2720378 GC + CC genotypes (OR = 1.39, 95% CI = 1.07-1.80, P = 0.014) or rs2069762 AC + CC genotypes (OR = 1.28, 95% CI = 0.98-1.67, P = 0.066), compared with their wild type counterparts. In classification and regression tree analysis, individuals carrying the combined genotypes of rs2720378 GC or CC genotype, rs2069762 CA or CC genotype and rs1561876 AA genotype exhibited the highest KD risk (OR = 2.12, 95% CI = 1.46-3.07, P < 0.001), compared with the lowest risk carriers of rs2720378 GG genotype. Moreover, a significant dose effect was observed among these three variants (Ptrend < 0.001). In conclusion, this study implicates that single- and multiple-risk genetic variants in this pathway might contribute to KD susceptibility. Further studies on more comprehensive single nucleotide polymorphisms, different ethnicities and larger sample sizes are warranted, and the exact biological mechanisms need to be further clarified.

Indexed as

BiomarkersCase-Control StudiesCaspase 3ChildFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMucocutaneous Lymph Node SyndromeNFATC Transcription FactorsPhosphotransferases (Alcohol Group Acceptor)Polymorphism, Single NucleotideRisk FactorsSignal TransductionBiomarkersCASP3 protein, humanCaspase 3Inositol 1,4,5-trisphosphate 3-kinaseNFATC Transcription FactorsPhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID24903211
PMCPMC4047536
OpenAlexW1987436442

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.