Abstract
Fetal growth restriction (FGR) is the failure of a fetus to reach its full genetic growth potential. It occurs in up to 8% of pregnancies, and after premature birth is the second leading cause of infant mortality and morbidity. There is no treatment currently available for FGR. Its primary cause, when not attributable to structural or genetic defects of the fetus, is ‘placental insufficiency’. This broad definition covers the inability of the fetus to acquire sufficient nutrients and oxygen, and is influenced by a number of factors including altered maternal or fetal blood flow, reduced nutrient transport or changes in the placenta such as increased barrier thickness inhibiting nutrient transfer. For those researchers studying FGR and developing new therapies, choosing an animal model is a crucial consideration. It is vital to clearly frame the question being asked, as this will impact the factor influencing fetal nutrient delivery in the model, and will also affect the applicability of the results to the human condition. This review examines the range of in vivo models of FGR available for those engaged in translational research.
Highlights
Fetal growth restriction (FGR) is a failure of a fetus to reach its full genetic growth potential
Fetal growth restriction with 25e40% reduction of visceral organ growth 40% die at birth from acute respiratory failure, similar to respiratory distress syndrome in humans Homozygous is embryonic lethal heterozygous results in fetal growth restriction Fetal growth restriction with brain sparing, hypoxia and reduced placental system A transport 30% fetal growth restriction with brain sparing Fetal growth restriction with adiposity Unilateral ovariectomy pre-pregnancy producing a normal size litter in single horn Differential blood flow results in fetal growth restriction in the middle fetuses
Trophoblast invasion is crucial to adequate supply of blood to the placenta, so the mouse would not be a suitable model for investigation into the causes of inadequate spiral artery remodelling, nor any interventions aimed at promoting trophoblast invasion
Summary
Fetal growth restriction (FGR) is a failure of a fetus to reach its full genetic growth potential. The primary cause of FGR, when not attributable to structural or genetic defects of the fetus, is ‘placental insufficiency’. This is a global term covering the failure of the fetus to acquire nutrients and oxygen adequate for its needs, and is influenced by a number of factors including altered maternal or fetal blood flow, reduced nutrient transport or changes in the placenta such as increased barrier thickness inhibiting nutrient transfer. When choosing an animal model in which to study FGR and to develop new therapies, it is important to clearly frame the question being asked, as this will have consequences for the factor influencing fetal nutrient delivery in the model, and for the applicability of the results to the human condition
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