Evidence map›Paper›PMID 38884756›Full record

ArticleAdvances in experimental medicine and biology2024

Human Genetics of Tricuspid Atresia and Univentricular Heart.

Abdul-Karim Sleiman, Liane Sadder, George Nemer

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Article 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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. 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

3 authors.

Abdul-Karim SleimanFaculty of Medicine, American University of Beirut, Beirut, Lebanon.
Liane SadderFaculty of Medicine, American University of Beirut, Beirut, Lebanon.
George NemerFaculty of Medicine, American University of Beirut, Beirut, Lebanon. gn08@aub.edu.lb.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tricuspid atresia (TA) is a rare congenital heart condition that presents with a complete absence of the right atrioventricular valve. Because of the rarity of familial and/or isolated cases of TA, little is known about the potential genetic abnormalities contributing to this condition. Potential responsible chromosomal abnormalities were identified in exploratory studies and include deletions in 22q11, 4q31, 8p23, and 3p as well as trisomies 13 and 18. In parallel, potential culprit genes include the ZFPM2, HEY2, NFATC1, NKX2-5, MYH6, and KLF13 genes. The aim of this chapter is to expose the genetic components that are potentially involved in the pathogenesis of TA in humans. The large variability in phenotypes and genotypes among cases of TA suggests a genetic network that involves many components yet to be unraveled.

Indexed as

Tricuspid AtresiaChromosome AberrationsHumansPhenotypeUniventricular Heart22q11 deletionAlagille syndromeASDAtrial septal defectAtrioventricular valveAV valveCardiac progenitor cellsEllis–van Creveld syndromeEndocardial cushionsEndocardiumEpicardiumFOG2HEY2KLF13MesodermMYH6MyocardiumNFATC1NKX2-5TGATransposition of the great arteriesTricuspid atresiaTrisomy 13Trisomy 18Univentricular heartVentricular septal defectVSDZFPM2

Identifiers

PMID38884756

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.