Funding outcome

Iron deficiency is the most common nutritional deficiency in the world, affecting an estimated one third of global population to some degree. Pregnant women and young children are among the most susceptible subgroups, due to the increased iron demands of pregnancy and of growth and development. We and others have shown that offspring that were iron deficient during pregnancy are at a greater risk of developing a host of complications in later life, including high blood pressure and abnormal kidney function. Due to its prevalence and tendency to affect pregnant women, iron deficiency is likely an important contributor to the burden of heart disease, stroke, and other cardiovascular diseases all over the world. To make matters worse, seemingly straight-forward interventions such as iron supplementation are often not effective in improving pregnancy outcomes associated with iron deficiency, and can even pose health problems for the mother and fetus. Therefore, new, safe and effective treatment strategies are urgently needed. Our past work has focused on understanding how iron deficiency during pregnancy impacts fetal growth and development, and its long-term effects of the cardiovascular system. We have identified dysfunction in the mitochondria, the powerplant of the cell, as an important mechanism linking early iron deficiency with increased risk of heart disease in later life. This proposal builds on our previous work. The objectives of this work are to understand how mitochondrial dysfunction impacts kidney development and long-term function, and to test the effectiveness of a mitochondrial-targeted antioxidant to reduce the damage caused by prenatal iron deficiency, and hence prevent and long-term cardiovascular dysfunction in these offspring.