Evidence map›Paper›PMID 35448089›Full record

ReviewJournal of cardiovascular development and disease2022

HLHS: Power of the Chick Model.

David Sedmera

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cardiovascular development and disease, 2022. 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
0.1field-weighted citation impact, top 59% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. The avian embryo as a time-honoured animal model in developmental, biomedical and agricultural research.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
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

1 author at 1 institution in 1 country.

David SedmeraInstitute of Anatomy, First Faculty of Medicine, Charles University, 128 00 Prague, Czech Republic.ORCID 0000-0002-6828-3671
Czech Academy of Sciences · CZ

Funding

Charles University PROGRES Q38, COOPERATIONCzech Academy of Sciences RVO: 67985823Czech Health Research Council NU21-02-00402Czech Science Foundation 22-05271S
6 · The paper itself

Abstract

backgroundHypoplastic left heart syndrome (HLHS) is a rare but deadly form of human congenital heart disease, most likely of diverse etiologies. Hemodynamic alterations such as those resulting from premature foramen ovale closure or aortic stenosis are among the possible pathways.

methodsThe information gained from studies performed in the chick model of HLHS is reviewed. Altered hemodynamics leads to a decrease in myocyte proliferation causing hypoplasia of the left heart structures and their functional changes.

conclusionsAlthough the chick phenocopy of HLHS caused by left atrial ligation is certainly not representative of all the possible etiologies, it provides many useful hints regarding the plasticity of the genetically normal developing myocardium under altered hemodynamic loading leading to the HLHS phenotype, and even suggestions on some potential strategies for prenatal repair.

Indexed as

embryonic myocardiumhemodynamic alterationleft atrial ligationleft ventricular hypoplasiamyocyte proliferation

Identifiers

PMID35448089
PMCPMC9031965
OpenAlexW4223429434

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.