Evidence map›Paper›PMID 28849223›Full record

ArticleMolecular medicine reports2017

Identification of TNFSF13, SPATC1L, SLC22A25 and SALL4 as novel susceptibility loci for atrial fibrillation by an exome‑wide association study.

Yoshiji Yamada, Jun Sakuma, Ichiro Takeuchi, Yoshiki Yasukochi, Kimihiko Kato, Mitsutoshi Oguri, Tetsuo Fujimaki, Hideki Horibe, Masaaki Muramatsu, Motoji Sawabe and 8 more

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

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

18 authors at 7 institutions in 1 country.

Yoshiji YamadaDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu 514‑8507, Japan.
Jun SakumaCREST, Japan Science and Technology Agency, Kawaguchi 332‑0012, Japan.
Ichiro TakeuchiCREST, Japan Science and Technology Agency, Kawaguchi 332‑0012, Japan.
Yoshiki YasukochiDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu 514‑8507, Japan.
Kimihiko KatoDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu 514‑8507, Japan.
Mitsutoshi OguriDepartment of Human Functional Genomics, Advanced Science Research Promotion Center, Mie University, Tsu 514‑8507, Japan.
Tetsuo FujimakiDepartment of Cardiovascular Medicine, Inabe General Hospital, Inabe 511‑0428, Japan.
Hideki HoribeDepartment of Cardiovascular Medicine, Gifu Prefectural Tajimi Hospital, Tajimi 507‑8522, Japan.
Masaaki MuramatsuDepartment of Molecular Epidemiology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101‑0062, Japan.
Motoji SawabeSection of Molecular Pathology, Graduate School of Health Care Sciences, Tokyo Medical and Dental University, Tokyo 113‑8510, Japan.
Yoshinori FujiwaraResearch Team for Social Participation and Community Health, Tokyo Metropolitan Institute of Gerontology, Tokyo 173‑0015, Japan.
Yu TaniguchiResearch Team for Social Participation and Community Health, Tokyo Metropolitan Institute of Gerontology, Tokyo 173‑0015, Japan.
Shuichi ObuchiResearch Team for Promoting Support System for Home Care, Tokyo Metropolitan Institute of Gerontology, Tokyo 173‑0015, Japan.
Hisashi KawaiResearch Team for Promoting Support System for Home Care, Tokyo Metropolitan Institute of Gerontology, Tokyo 173‑0015, Japan.
Shoji ShinkaiResearch Team for Social Participation and Health Promotion, Tokyo Metropolitan Institute of Gerontology, Tokyo 173‑0015, Japan.
Seijiro MoriCenter for Promotion of Clinical Investigation, Tokyo Metropolitan Geriatric Hospital, Tokyo 173‑0015, Japan.
Tomio AraiDepartment of Pathology, Tokyo Metropolitan Geriatric Hospital, Tokyo 173‑0015, Japan.
Masashi TanakaDepartment of Clinical Laboratory, Tokyo Metropolitan Geriatric Hospital, Tokyo 173‑0015, Japan.
Tokyo Metropolitan Institute of Gerontology · JPMie University · JPTokyo Metropolitan Geriatric Hospital · JPJapan Science and Technology Agency · JPTokyo Medical and Dental University · JPGifu Prefectural Tajimi Hospital · JPShowa Inan General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An exome‑wide association study (EWAS) was performed to identify genetic variants, particularly low‑frequency or rare coding variants with a moderate to large effect size, that confer susceptibility to atrial fibrillation in Japanese. The EWAS for atrial fibrillation was performed with 13,166 subjects (884 patients with atrial fibrillation and 12,282 controls) using an Illumina HumanExome‑12 DNA Analysis BeadChip or Infinium Exome‑24 BeadChip arrays. The association of atrial fibrillation with allele frequencies of 41,243 single nucleotide polymorphisms (SNPs) that passed quality control was examined with Fisher's exact test. Based on Bonferroni's correction, a P<1.21x10‑6 was considered statistically significant. The EWAS for atrial fibrillation revealed that 122 SNPs were significantly associated with this condition. The association of the identified SNPs to atrial fibrillation was further examined by multivariable logistic regression analysis with adjustment for age, sex and the prevalence of hypertension. Eight SNPs were related (P<0.01) to atrial fibrillation, among which three polymorphisms, rs11552708 [G/A (G67R)]of TNF superfamily member 13 (TNFSF13; dominant model; P=9.36x10‑9; odds ratio, 0.58), rs113710653 [C/T (E231 K)] of spermatogenesis and centriole associated 1 like (SPATC1L; dominant model; P=1.09x10‑5; odds ratio, 3.27), and rs11231397 [G/C (R300T)] of solute carrier family 22 member 25 (SLC22A25; additive model; P=3.71x10‑5; odds ratio, 1.77), were significantly (P<1.02x10‑4) associated with this condition. The minor T allele of rs113710653 and the minor C allele of rs11231397 were risk factors for atrial fibrillation, whereas the minor A allele of rs11552708 was protective against this condition. In addition, rs77538589 [C/T (G117R)] of SALL4 exhibited a tendency to be associated with atrial fibrillation (dominant model; P=0.0002; odds ratio, 1.88), with the minor T allele representing a risk factor for this condition. TNFSF13, SPATC1L, SLC22A25 and SALL4 may thus be novel susceptibility loci for atrial fibrillation in the Japanese population.

Indexed as

AgedAtrial FibrillationCase-Control StudiesCytoskeletal ProteinsExomeFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiddle AgedOrganic Cation Transport ProteinsPolymorphism, Single NucleotideRisk FactorsSolute Carrier ProteinsTranscription FactorsCytoskeletal ProteinsOrganic Cation Transport ProteinsSALL4 protein, humanSLC22A25 protein, humanSolute Carrier ProteinsSPATC1L protein, humanTNFSF13 protein, humanTranscription FactorsTumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID28849223
PMCPMC5865780
OpenAlexW2745602859

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.