Evidence map›Paper›PMID 25875170›Full record

SynthesisPloS one2015

Association between the European GWAS-identified susceptibility locus at chromosome 4p16 and the risk of atrial septal defect: a case-control study in Southwest China and a meta-analysis.

Li Zhao, Bei Li, Ke Dian, Binwu Ying, Xiaojun Lu, Xuejiao Hu, Qi An, Chunxia Chen, Chunyan Huang, Bin Tan and 1 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Human Genetics of Atrial Septal Defect.Advances in experimental medicine and biology · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. 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

11 authors at 2 institutions in 1 country.

Li ZhaoDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Bei LiDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Ke DianDepartment of Cardiothoracic Surgery, West China Hospital, Sichuan University, Chengdu, P.R. China.
Binwu YingDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Xiaojun LuDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Xuejiao HuDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Qi AnDepartment of Cardiothoracic Surgery, West China Hospital, Sichuan University, Chengdu, P.R. China.
Chunxia ChenDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Chunyan HuangDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Bin TanDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Li QinDepartment of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, P. R. China.
Sichuan University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial septal defect (ASD) is the third most frequent type of congenital heart anomaly, featuring shunting of blood between the two atria. Gene-environment interaction remains to be an acknowledged cause for ASD occurrence. A recent European genome-wide association study (GWAS) of congenital heart disease (CHD) identified 3 susceptibility SNPs at chromosome 4p16 associated with ASD: rs870142, rs16835979 and rs6824295. A Chinese-GWAS of CHD conducted in the corresponding period did not reveal the 3 susceptibility SNPs, but reported 2 different risk SNPs: rs2474937 and rs1531070. Therefore, we aimed to investigate the associations between the 3 European GWAS-identified susceptibility SNPs and ASD risk in the Han population in southwest China. Additionally, to increase the robustness of our current analysis, we conducted a meta-analysis combining published studies and our current case-control study. We performed association, linkage disequilibrium, and haplotype analysis among the 3 SNPs in 190 ASD cases and 225 age-, sex-, and ethnicity-matched healthy controls. Genotype and allele frequencies among the 3 SNPs showed statistically significant differences between the cases and controls. Our study found that individuals carrying the allele T of rs870142, the allele A of rs16835979, and the allele T of rs6824295 had a respective 50.1% (odds ratio (OR) = 1.501, 95% confidence interval (CI) = 1.122-2.009, PFDR-BH = 0.018), 48.5% (OR = 1.485, 95%CI = 1.109-1.987, PFDR-BH = 0.012), and 38.6% (OR = 1.386, 95%CI = 1.042-1.844, PFDR-BH = 0.025) increased risk to develop ASD than wild-type allele carriers in our study cohort. In the haplotype analysis, we identified a disease-risk haplotype (TAT) (OR = 1.540, 95%CI = 1.030-2.380, PFDR-BH = 0.016). Our meta-analysis also showed that the investigated SNP was associated with ASD risk (combined OR (95%CI) = 1.35 (1.24-1.46), P < 0.00001). Our study provides compelling evidence to motivate better understanding of the etiology of ASD.

Indexed as

Genetic LociGenetic Predisposition to DiseaseGenome-Wide Association StudyCase-Control StudiesChinaChromosomes, Human, Pair 4EuropeFemaleHaplotypesHeart Septal Defects, AtrialHumansLinkage DisequilibriumMalePolymorphism, Single NucleotideRisk FactorsYoung Adult

Identifiers

PMID25875170
PMCPMC4395394
OpenAlexW1987603786

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.