Funding outcome

A common problem in pregnancy is that the fetus does not receive enough oxygen (called hypoxia). This can affect fetal growth, which we now know leads to long-term health risks for the child including an increased risk of adult cardiovascular disease. In a model system, we have previously shown impaired function of the heart in adult male and female offspring who had been exposed to hypoxia as a fetus. However, why this happens is not known. We suspect that an important part of the cell, called the mitochondria, may play a key role. Mitochondria are the energy source to the cell and thus essential for proper heart function. When the function of the mitochondria is impaired, it releases damaging molecules into the cell, which eventually lead to cell damage. In this study, we aim to study the role of these mitochondria, and the damaging molecules they release, in the heart dysfunction that is observed in offspring born from hypoxia pregnancies. In addition, as there are many sex differences in the function of the mitochondria, we aim to see if there are differences between male and female offspring. To assess this, we will look at mitochondrial function in the hearts, and we will assess the role of the damaging molecules in heart function and in the blood vessels of the heart, in our model system of adult male and female rat offspring exposed to hypoxia at the end of pregnancy. Our study will contribute to our knowledge of why complicated pregnancies lead to impaired cardiovascular health in the offspring, with the goal to develop early targeted and sex specific therapies to improve children's health outcomes later in life.