Jeremy A. Hansell

TL;DR: It is tested the hypothesis that oxidative stress in the fetal heart and vasculature underlies the molecular basis via which prenatal hypoxia programmes cardiovascular dysfunction in later life and possible targets for intervention against developmental origins of cardiac and peripheral vascular dysfunction in offspring of risky pregnancy.

TL;DR: The data show that in pregnancy complicated by undernutrition, melatonin may improve placental efficiency and birth weight by upregulating placental antioxidant enzymes.

TL;DR: Developmental hypoxia or undernutrition in late gestation has differential effects on fetal cardiovascular morphology and function, and both hypoxic and undernourished pregnancy was associated with asymmetric fetal growth restriction.

TL;DR: Findings link prenatal hypoxia to down‐regulation of components of hepatic and muscle Akt expression in adult offspring to represent a pharmaceutical target for clinical intervention against the developmental programming of metabolic disease resulting from prenatal Hypoxia.

TL;DR: This chapter reviews how fetal chronic hypoxia programmes cardiac and endothelial dysfunction in the offspring in adult life and discusses the mechanisms via which this may occur, and offers both insight into mechanisms and possible therapeutic targets for clinical intervention against the early origin of cardiometabolic disease in pregnancy complicated by fetal chronic Hypoxia.