skip to content

Centre for Trophoblast Research


Developmental origins of heart disease

Supervisor: Professor Dino A. Giussani, Department of Physiology Development and Neuroscience


Heart disease kills 1 in 3 people in the developed world, imposing a vast burden on health and wealth. We know that the interaction between genetic make-up and environmental risk factors, such as smoking, obesity or a sedentary life increase the risk of heart disease.  It has also become established that the gene-environment interaction before birth may be just as, if not more important than the gene-environment interaction after birth in shaping the risk of future heart health.  This clearly makes a lot of sense because our physiology is so much more plastic and susceptible to environmental influences during early life.  Therefore, it is now established that adverse conditions during pregnancy can also increase the risk of future heart disease in the adult offspring, a concept known as developmental programming.  However, the mechanisms underlying this early origin of cardiovascular disease in complicated pregnancy remain unknown.


One of the most common complications during pregnancy is chronic fetal hypoxia, as may occur during pre-eclampsia or placental insufficiency.  Our laboratory has shown in large (sheep) and small (rats and chick embryos) animal species that hypoxic development can trigger early origins of cardiac and endothelial dysfunction in fetal and adult offspring secondary to the genesis of oxidative stress.  Therefore, antioxidant therapy in development complicated by chronic fetal hypoxia may prove protective. 


In this project, students will assess cardiac (Langendorff/Echocardiography/Stereology) and vascular (wire myography/histology/molecular biology) morphology and function in fetal or adult offspring from control or hypoxic development with and without different antioxidant therapies.    


For further information, please do not hesitate to contact me: