Evidence map›Paper›PMID 38884726›Full record

ReviewAdvances in experimental medicine and biology2024

Human Genetics of Atrial Septal Defect.

Lars A Larsen, Marc-Phillip Hitz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

2 authors.

Lars A LarsenDepartment of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark.
Marc-Phillip HitzInstitute of Medical Genetics, University Medicine Oldenburg, Oldenburg, Germany. Hitz.Marc-Phillip@klinikum-oldenburg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although atrial septal defects (ASD) can be subdivided based on their anatomical location, an essential aspect of human genetics and genetic counseling is distinguishing between isolated and familiar cases without extracardiac features and syndromic cases with the co-occurrence of extracardiac abnormalities, such as developmental delay. Isolated or familial cases tend to show genetic alterations in genes related to important cardiac transcription factors and genes encoding for sarcomeric proteins. By contrast, the spectrum of genes with genetic alterations observed in syndromic cases is diverse. Currently, it points to different pathways and gene networks relevant to the dysregulation of cardiomyogenesis and ASD pathogenesis. Therefore, this chapter reflects the current knowledge and highlights stable associations observed in human genetics studies. It gives an overview of the different types of genetic alterations in these subtypes, including common associations based on genome-wide association studies (GWAS), and it highlights the most frequently observed syndromes associated with ASD pathogenesis.

Indexed as

Genome-Wide Association StudyHeart Septal Defects, AtrialGenetic Predisposition to DiseaseHumansMutationACTC1ASDASD 2Atrial septal defectAtrioventricular septum defectsBRAFCardio-facio-cutaneous syndromeCardiomyogenesisCDK13CHARGE syndromeCHD4CHD7DHCR7endoMTFamilial ASDG6PC3GATA4GATA binding protein (GATA)GATA4Genome-wide association studiesHolt-Oram syndromeIsolated ASDKabuki syndromeKMT2DMAP2K1MAP2K2Mowat-Wilson syndromeMYH6Myosin heavy chain (MYH)MYH6NKX2-5Noonan syndromePatent foramen ovalePEX7PFOPrimum atrial septal defectsPTPN11RBM10Rhizomelic chondrodysplasia punctataSecundum atrial septal defectsSifrim-Hitz-Weiss syndromeSinus venosus defectsSmith–Lemli–Opitz syndromeSporadic ASDSyndromic ASDTARP syndromeTBX20T-box (TBX)TBX20TBX5ZEB2

Identifiers

What OpenQuestion holds

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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.