Evidence map›Paper›PMID 30402224›Full record

ArticleBiomedical reports2018

Identification of 26 novel loci that confer susceptibility to early-onset coronary artery disease in a Japanese population.

Yoshiji Yamada, Yoshiki Yasukochi, Kimihiko Kato, Mitsutoshi Oguri, Hideki Horibe, Tetsuo Fujimaki, Ichiro Takeuchi, Jun Sakuma

Open access · diamondAbstract read
In one paragraph

Article in Biomedical reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 3 syntheses or guidelines pooled it, 38 citations in OpenAlex.

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  13. Involvement of FAM170B-AS1, hsa-miR-1202, and hsa-miR-146a-5p in breast cancer.Cancer biomarkers : section A of Disease markers · 2024
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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

8 authors at 3 institutions in 1 country.

Yoshiji YamadaDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu, Mie 514-8507, Japan.
Yoshiki YasukochiDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu, Mie 514-8507, Japan.
Kimihiko KatoDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu, Mie 514-8507, Japan.
Mitsutoshi OguriDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu, Mie 514-8507, Japan.
Hideki HoribeDepartment of Cardiovascular Medicine, Gifu Prefectural Tajimi Hospital, Tajimi, Gifu 507-8522, Japan.
Tetsuo FujimakiDepartment of Cardiovascular Medicine, Northern Mie Medical Center Inabe General Hospital, Inabe, Mie 511-0428, Japan.
Ichiro TakeuchiCREST, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan.
Jun SakumaCREST, Japan Science and Technology Agency, Kawaguchi, Saitama 332-0012, Japan.
Mie University · JPJapan Science and Technology Agency · JPGifu Prefectural Tajimi Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early-onset coronary artery disease (CAD) has a strong genetic component. Although genome-wide association studies have identified various genes and loci significantly associated with CAD mainly in European populations, genetic variants that contribute toward susceptibility to this condition in Japanese patients remain to be definitively identified. In the present study, exome-wide association studies (EWASs) were performed to identify genetic variants that confer susceptibility to early-onset CAD in Japanese. A total of 7,256 individuals aged ≤65 years were enrolled in the present study. EWAS were conducted on 1,482 patients with CAD and 5,774 healthy controls. Genotyping of single nucleotide polymorphisms (SNPs) was performed using Illumina Human Exome-12 DNA Analysis BeadChip or Infinium Exome-24 BeadChip arrays. The association between allele frequencies for 31,465 SNPs that passed quality control and CAD was examined using Fisher's exact test. To compensate for multiple comparisons of allele frequencies with CAD, a false discovery rate (FDR) of <0.05 was applied for statistically significant associations. The association between allele frequencies for 31,465 SNPs and CAD, as determined by Fisher's exact test, demonstrated that 170 SNPs were significantly (FDR <0.05) associated with CAD. Multivariable logistic regression analysis with adjustment for age, sex, and the prevalence of hypertension, diabetes mellitus and dyslipidemia revealed that 162 SNPs were significantly (P<0.05) associated with CAD. A stepwise forward selection procedure was performed to examine the effects of genotypes for the 162 SNPs on CAD. The 54 SNPs were significant (P<0.05) and independent [coefficient of determination (R

Indexed as

coronary artery diseaseexome-wide association studygeneticsischemic heart diseasemyocardial infarction

Identifiers

PMID30402224
PMCPMC6201041
OpenAlexW2890814659

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.