Evidence map›Paper›PMID 28758112›Full record

Trial reportBioMed research international2017

Parental Genetic Variants, MTHFR 677C>T and MTRR 66A>G, Associated Differently with Fetal Congenital Heart Defect.

Qian-Nan Guo, Hong-Dan Wang, Li-Zhen Tie, Tao Li, Hai Xiao, Jian-Gang Long, Shi-Xiu Liao

Open access · hybridAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. The roles ofBioscience reports · 2018
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Effects of Gender Differences inInternational journal of genomics · 2025
    Article
  6. Article
  7. Genes · 2023
    Article
  8. A Common Polymorphism in theJournal of cardiovascular development and disease · 2022
    Article
  9. Article
  10. 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

7 authors at 2 institutions in 1 country.

Qian-Nan GuoThe Medical Genetic Center, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0003-4680-8868
Hong-Dan WangThe Medical Genetic Center, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0001-6498-9979
Li-Zhen TieDepartment of Cardiology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0002-9890-2074
Tao LiThe Medical Genetic Center, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.
Hai XiaoThe Medical Genetic Center, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0001-9263-2686
Jian-Gang LongCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.ORCID 0000-0002-6584-3880
Shi-Xiu LiaoThe Medical Genetic Center, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou 450000, China.ORCID 0000-0002-7173-7654
Zhengzhou University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCongenital heart defect (CHD) is one of the most common birth defects in the world. The methylenetetrahydrofolate reductase (MTHFR) and methionine synthase reductase (MTRR) genes are two of the most important candidate genes for fetal CHD. However, the correlations between the two genes and fetal CHD were inconsistent in various reports. Therefore, this study is aimed to evaluate the parental effects of the two genes on fetal CHD via three genetic polymorphisms, MTHFR 677C>T (rs1801133), MTHFR 1298 A>C (rs1801131), and MTRR 66A>G (rs1801394).

methodsParents with pregnancy history of fetal CHD were divided into two subgroups: ventricular septal defect (VSD) (21) and non-VSD groups (78). VSD, non-VSD, and 114 control parents (controls) were analyzed in this study. Genotyping of these genetic polymorphisms was done by sequencing.

resultsThe MTHFR 677C>T polymorphism of either mothers or fathers was independently associated with fetal non-VSD (

conclusionIn either maternal or paternal group, the MTHFR 677C>T polymorphism was independently related to fetal non-VSD, while the MTRR 66A>G polymorphism was independently related to fetal VSD.

Indexed as

FetusPolymorphism, GeneticAdultFemaleFerredoxin-NADP ReductaseHeart Septal DefectsHumansMaleMethylenetetrahydrofolate Reductase (NADPH2)Ferredoxin-NADP Reductasemethionine synthase reductaseMethylenetetrahydrofolate Reductase (NADPH2)MTHFR protein, human

Identifiers

PMID28758112
PMCPMC5512027
OpenAlexW2730556650

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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.