Evidence map›Paper›PMID 41811217›Full record

ReviewThe Journal of physiology2026

Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease.

Melanie R Bertossa, Jack R T Darby, Ashley S Meakin, Mitchell C Lock, Steven K S Cho, Christopher K Macgowan, Mike Seed, Michael D Wiese, Janna L Morrison

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Journal of physiology, 2026. 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

9 authors.

Melanie R BertossaEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Jack R T DarbyEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Ashley S MeakinEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Mitchell C LockEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Steven K S ChoEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Christopher K MacgowanTranslational Medicine, Hospital for Sick Children, Toronto, Canada.
Mike SeedDivision of Cardiology, Hospital for Sick Children, Toronto, Canada.
Michael D WieseEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.
Janna L MorrisonEarly Origins of Adult Health Research Group, Robinson Research Institute, School of Pharmacy and Biomedical Sciences, College of Health, Adelaide University, Adelaide, Australia.

Funding

ASM was funded by a National Heart Foundation Postdoctoral Fellowship 108157-2024_PDFJLM was funded by an ARC Future Fellowship and a NHMRC Investigator Grant Leader2;GNT2041967JLM was funded by an ARC Future Fellowship and a NHMRC Investigator Grant Level3;FT170100431JRTD was funded by a University of South Australia Enterprise Postdoctoral Fellowship.MCL was funded by a fellowship from the Lloyd Cox O&G Research Fund.MRB was funded by a University of South Australia Research Scholarship.
6 · The paper itself

Abstract

Depending on the pregnancy complication, substrate delivery to a developing fetus can be reduced, changing the course of fetal growth below the genetically determined in utero growth potential, resulting in fetal growth restriction (FGR). FGR is linked to an increased risk of developing cardiovascular disease (CVD) in later life. When caused by placental insufficiency, FGR is characterized by fetal hypoxaemia and hypoglycaemia due to reduced substrate supply to the fetus. However, other common pregnancy complications exist, where fetal hypoxaemia or hypoglycaemia may or may not occur. It is therefore necessary to understand the independent and synergistic contributions of hypoxaemia and hypoglycaemia to the fetal origins of CVD. In doing so, this knowledge will aid in the development of intervention strategies. The aim of this review is to provide mechanistic insights by comparing findings across different paradigms of developmental programming using animal models of FGR, with consideration of the timing, duration, and severity of the insult, and the ventricles and fetal sex studied.

Indexed as

Cardiovascular DiseasesFetal Growth RetardationNutrientsOxygenAnimalsDevelopmental Origins of Health and DiseaseDisease Models, AnimalFemaleHumansPregnancyOxygencardiovascular diseasefetalgrowth restrictionheartnutrientsoxygen

Identifiers

PMID41811217
PMCPMC13481021

What Socratic 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 Socratic graph.