Evidence map›Paper›PMID 24400145›Full record

ArticlePhysiological reports2013

Multimodal imaging reveals a role for Akt1 in fetal cardiac development.

Katrien Vandoorne, Moriel H Vandsburger, Karen Weisinger, Vlad Brumfeld, Brian A Hemmings, Alon Harmelin, Michal Neeman

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Role of circulating microRNAs in tetralogy of Fallot.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2025
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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

7 authors at 3 institutions in 3 countries.

Katrien VandoorneBiological Regulation, Weizmann Institute of Science Rehovot, Israel ; Biomedical engineering, Eindhoven University of Technology Eindhoven, The Netherlands.
Moriel H VandsburgerBiological Regulation, Weizmann Institute of Science Rehovot, Israel.
Karen WeisingerBiological Regulation, Weizmann Institute of Science Rehovot, Israel.
Vlad BrumfeldChemical Research Support, Weizmann Institute of Science Rehovot, Israel.
Brian A HemmingsFriedrich Miescher Institute for Biomedical Research Basel, Switzerland.
Alon HarmelinVeterinary Resources, Weizmann Institute of Science Rehovot, Israel.
Michal NeemanBiological Regulation, Weizmann Institute of Science Rehovot, Israel.
Weizmann Institute of Science · ILEindhoven University of Technology · NLFriedrich Miescher Institute · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Even though congenital heart disease is the most prevalent malformation, little is known about how mutations affect cardiovascular function during development. Akt1 is a crucial intracellular signaling molecule, affecting cell survival, proliferation, and metabolism. The aim of this study was to determine the role of Akt1 on prenatal cardiac development. In utero echocardiography was performed in fetal wild-type, heterozygous, and Akt1-deficient mice. The same fetal hearts were imaged using ex vivo micro-computed tomography (μCT) and histology. Neonatal hearts were imaged by in vivo magnetic resonance imaging. Additional ex vivo neonatal hearts were analyzed using histology and real-time PCR of all three groups. In utero echocardiography revealed abnormal blood flow patterns at the mitral valve and reduced contractile function of Akt1 null fetuses, while ex vivo μCT and histology unraveled structural alterations such as dilated cardiomyopathy and ventricular septum defects in these fetuses. Further histological analysis showed reduced myocardial capillaries and coronary vessels in Akt1 null fetuses. At neonatal age, Akt1-deficient mice exhibited reduced survival with reduced endothelial cell density in the myocardium and attenuated cardiac expression of vascular endothelial growth factor A and collagen Iα1. To conclude, this study revealed a central role of Akt1 in fetal cardiac function and myocardial angiogenesis inducing fetal cardiomyopathy and reduced neonatal survival. This study links a specific physiological phenotype with a defined genotype, namely Akt1 deficiency, in an attempt to pinpoint intrinsic causes of fetal cardiomyopathies.

Indexed as

Akt1echocardiographyfetusheartmice

Identifiers

PMID24400145
PMCPMC3871458
OpenAlexW2028177373

What OpenQuestion holds

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LicenceCC BY
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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.