Evidence map›Paper›PMID 26110764›Full record

ArticlePloS one2015

Characterization of SMAD3 Gene Variants for Possible Roles in Ventricular Septal Defects and Other Congenital Heart Diseases.

Fei-Feng Li, Jing Zhou, Dan-Dan Zhao, Peng Yan, Xia Li, Ying Han, Xian-Shu Li, Gui-Yu Wang, Kai-Jiang Yu, Shu-Lin Liu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 28 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

10 authors at 3 institutions in 2 countries.

Fei-Feng LiGenomics Research Center (one of the State-Province Key Laboratory of Biopharmaceutical Engineering, China), Harbin Medical University, Harbin, China.
Jing ZhouIntensive Care Unit, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Dan-Dan ZhaoGenomics Research Center (one of the State-Province Key Laboratory of Biopharmaceutical Engineering, China), Harbin Medical University, Harbin, China.
Peng YanDepartment of Colorectal Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xia LiGenomics Research Center (one of the State-Province Key Laboratory of Biopharmaceutical Engineering, China), Harbin Medical University, Harbin, China.
Ying HanGenomics Research Center (one of the State-Province Key Laboratory of Biopharmaceutical Engineering, China), Harbin Medical University, Harbin, China.
Xian-Shu LiDaqing People's Hospital, Daqing, China.
Gui-Yu WangDepartment of Colorectal Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Kai-Jiang YuIntensive Care Unit, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shu-Lin LiuGenomics Research Center (one of the State-Province Key Laboratory of Biopharmaceutical Engineering, China), Harbin Medical University, Harbin, China; Department of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, Canada.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CNUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNodal/TGF signaling pathway has an important effect at early stages of differentiation of human embryonic stem cells in directing them to develop into different embryonic lineages. SMAD3 is a key intracellular messenger regulating factor in the Nodal/TGF signaling pathway, playing important roles in embryonic and, particularly, cardiovascular system development. The aim of this work was to find evidence on whether SMAD3 variations might be associated with ventricular septal defects (VSD) or other congenital heart diseases (CHD).

methodsWe sequenced the SMAD3 gene for 372 Chinese Han CHD patients including 176 VSD patients and evaluated SNP rs2289263, which is located before the 5'UTR sequence of the gene. The statistical analyses were conducted using Chi-Square Tests as implemented in SPSS (version 13.0). The Hardy-Weinberg equilibrium test of the population was carried out using the online software OEGE.

resultsThree heterozygous variants in SMAD3 gene, rs2289263, rs35874463 and rs17228212, were identified. Statistical analyses showed that the rs2289263 variant located before the 5'UTR sequence of SMAD3 gene was associated with the risk of VSD (P value=0.013 <0.05).

conclusionsThe SNP rs2289263 in the SMAD3 gene is associated with VSD in Chinese Han populations.

Indexed as

AdolescentAdultAgedAsian PeopleChildChild, PreschoolChinaFemaleGene FrequencyGenetic Association StudiesGenetic Predisposition to DiseaseHeartHeart Septal Defects, VentricularHumansInfantMaleNodal ProteinNODAL protein, humanSmad3 ProteinSMAD3 protein, human

Identifiers

PMID26110764
PMCPMC4482402
OpenAlexW2338554803

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.