Evidence map›Paper›PMID 29104469›Full record

ArticleInternational journal of medical sciences2017

MEF2C loss-of-function mutation contributes to congenital heart defects.

Xiao-Hui Qiao, Fei Wang, Xian-Ling Zhang, Ri-Tai Huang, Song Xue, Juan Wang, Xing-Biao Qiu, Xing-Yuan Liu, Yi-Qing Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Modelling Tetralogy of Fallot: insights and limitations of animal models.Frontiers in cell and developmental biology · 2026
    Review
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  8. Discovery ofAmerican journal of translational research · 2024
    Article
  9. Identification ofDiagnostics (Basel, Switzerland) · 2022
    Article
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  14. Article
  15. Journal of cardiovascular and thoracic research · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Article
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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

9 authors at 6 institutions in 1 country.

Xiao-Hui QiaoDepartment of Pediatric Internal Medicine, Ningbo Women & Children's Hospital, 339 Liuding Street, Ningbo 315012, China.
Fei WangDepartment of Neurosurgery, Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, China.
Xian-Ling ZhangDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, China.
Ri-Tai HuangDepartment of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 1630 Dongfang Road, Shanghai 200127, China.
Song XueDepartment of Cardiovascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 1630 Dongfang Road, Shanghai 200127, China.
Juan WangDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China.
Xing-Biao QiuDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huaihai Road, Shanghai 200030, China.
Xing-Yuan LiuDepartment of Pediatrics, Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, China.
Yi-Qing YangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 West Huaihai Road, Shanghai 200030, China.
Shanghai Jiao Tong University · CNTongji Hospital · CNRenji Hospital · CNShanghai Chest Hospital · CNShanghai East Hospital · CNShanghai Tenth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital heart disease (CHD) is the most common type of developmental abnormality in humans, and is a leading cause for substantially increased morbidity and mortality in affected individuals. Increasing studies demonstrates a pivotal role of genetic defects in the pathogenesis of CHD, and presently mutations in more than 60 genes have been associated with CHD. Nevertheless, CHD is of pronounced genetic heterogeneity, and the genetic basis underpinning CHD in a large proportion of patients remains unclear. In the present study, the whole coding exons and splicing donors/acceptors of the

Indexed as

AdolescentAmino Acid SequenceChildChild, PreschoolExonsFemaleGATA4 Transcription FactorHeart Defects, CongenitalHeterozygoteHumansInfantInfant, NewbornMaleMEF2 Transcription FactorsMutationMutation, MissenseGATA4 protein, humanGATA4 Transcription FactorMEF2C protein, humanMEF2 Transcription FactorsCongenital heart diseaseGeneticsMEF2CReporter gene assayTranscription factor

Identifiers

PMID29104469
PMCPMC5666546
OpenAlexW2754696183

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.