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Review
. 2026 Mar 11.
doi: 10.1113/JP289670. Online ahead of print.

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

Melanie R Bertossa  1 , Jack R T Darby  1 , Ashley S Meakin  1 , Mitchell C Lock  1 , Steven K S Cho  1   2 , Christopher K Macgowan  3   4 , Mike Seed  5   6 , Michael D Wiese  1 , Janna L Morrison  1   2   3
Affiliations
Review

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

Melanie R Bertossa et al. J Physiol. .

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.

Keywords: cardiovascular disease; fetal; growth restriction; heart; nutrients; oxygen.

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References

    1. Aguilera‐Méndez, A., Figueroa‐Fierros, I., Ruiz‐Pérez, X., Godínez‐Hernández, D., Saavedra‐Molina, A., Rios‐Chavez, P., Villafaña, S., Boone‐Villa, D., Ortega‐Cuellar, D., Gauthereau‐Torres, M. Y., Nieto‐Aguilar, R., & Palomera‐Sanchez, Z. (2024). The beneficial effects of prenatal biotin supplementation in a rat model of intrauterine caloric restriction to prevent cardiometabolic risk in adult female offspring. International Journal of Molecular Sciences, 25(16), 9052.
    1. Ahmadzadeh, E., Dudink, I., Walker, D. W., Sutherland, A. E., Pham, Y., Stojanovska, V., Polglase, G. R., Miller, S. L., & Allison, B. J. (2024). The medullary serotonergic centres involved in cardiorespiratory control are disrupted by fetal growth restriction. The Journal of Physiology, 602(21), 5923–5941.
    1. Al‐Hasan, Y. M., Evans, L. C., Pinkas, G. A., Dabkowski, E. R., Stanley, W. C., & Thompson, L. P. (2013). Chronic hypoxia impairs cytochrome oxidase activity via oxidative stress in selected fetal Guinea pig organs. Reproductive Sciences, 20(3), 299–307.
    1. Al‐Hasan, Y. M., Pinkas, G. A., & Thompson, L. P. (2014). Prenatal hypoxia reduces mitochondrial protein levels and cytochrome c oxidase activity in offspring Guinea pig hearts. Reproductive Sciences, 21(7), 883–891.
    1. Aláez, C., Calvo, R., Obregón, M. J., & Pascual‐Leone, A. M. (1992). Thyroid hormones and 5′‐deiodinase activity in neonatal undernourished rats. Endocrinology, 130, 773–779.

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