Evidence map›Paper›PMID 21297937›Full record

ArticlePloS one2011

Maternal genome-wide DNA methylation patterns and congenital heart defects.

Shimul Chowdhury, Stephen W Erickson, Stewart L MacLeod, Mario A Cleves, Ping Hu, Mohammad A Karim, Charlotte A Hobbs

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Epigenetics in Congenital Heart Disease.Journal of the American Heart Association · 2022
    Review
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  12. Article
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  16. Article
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  18. Intrauterine Programming of Diabetes Induced Cardiac Embryopathy.Diabetes & obesity international journal · 2019
    Article
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  20. 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.

Shimul ChowdhuryDepartment of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences, Arkansas Children's Hospital Research Institute, Little Rock, Arkansas, United States of America. schowdhury@uams.edu
Stephen W Erickson
Stewart L MacLeod
Mario A Cleves
Ping Hu
Mohammad A Karim
Charlotte A Hobbs
Arkansas Children's Hospital · USUniversity of Arkansas for Medical Sciences · US

Funding

Genomic/Epigenomic Factors and Non-Syndromic Congenital Heart Defect Risk R01HD039054 · NICHD · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI HOBBS, CHARLOTTE A · 2000 to 2016
$13.6M
CTRS. OF EXCELL. FOR SUR., RES. SERVICE &EVAL. AIMED AT BIRTH DEFECTSU50DD613236 · DD · ARKANSAS CHILDREN'S HOSP (LITTLE ROCK) · PI HOBBS, CHARLOTTE · 1997 to 2008
$2.2M
NCBDD CDC HHS 3-U50DD613236-10W1NCBDD CDC HHS U50 DD613236NICHD NIH HHS 5-R01-HD039054-08NICHD NIH HHS R01 HD039054
6 · The paper itself

Abstract

The majority of congenital heart defects (CHDs) are thought to result from the interaction between multiple genetic, epigenetic, environmental, and lifestyle factors. Epigenetic mechanisms are attractive targets in the study of complex diseases because they may be altered by environmental factors and dietary interventions. We conducted a population based, case-control study of genome-wide maternal DNA methylation to determine if alterations in gene-specific methylation were associated with CHDs. Using the Illumina Infinium Human Methylation27 BeadChip, we assessed maternal gene-specific methylation in over 27,000 CpG sites from DNA isolated from peripheral blood lymphocytes. Our study sample included 180 mothers with non-syndromic CHD-affected pregnancies (cases) and 187 mothers with unaffected pregnancies (controls). Using a multi-factorial statistical model, we observed differential methylation between cases and controls at multiple CpG sites, although no CpG site reached the most stringent level of genome-wide statistical significance. The majority of differentially methylated CpG sites were hypermethylated in cases and located within CpG islands. Gene Set Enrichment Analysis (GSEA) revealed that the genes of interest were enriched in multiple biological processes involved in fetal development. Associations with canonical pathways previously shown to be involved in fetal organogenesis were also observed. We present preliminary evidence that alterations in maternal DNA methylation may be associated with CHDs. Our results suggest that further studies involving maternal epigenetic patterns and CHDs are warranted. Multiple candidate processes and pathways for future study have been identified.

Indexed as

DNA MethylationGenome-Wide Association StudyCase-Control StudiesCpG IslandsFemaleFetal DevelopmentGenome, HumanHeart Defects, CongenitalHumansMothersPregnancy

Identifiers

PMID21297937
PMCPMC3031146
OpenAlexW2083957244

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.