Although better treatments are available, heart disease still affects a large number of people, as do obesity and diabetes. Sadly it now touches increasingly younger people. The foetal environment, obesity, diabetes and blood lipids (cholesterol) are among the most important risk factors for heart disease. Although we know that heart disease runs in families, the genetic mechanisms involved have not yet been clearly identified. Clinical observations suggest that epigenetic factors may be an important piece of the puzzle. Epigenetics refers to DNA modifications acting as an accelerator (gas pedal) or a constraint (break pedal) to gene readings (expression). Since the speed at which gene reading takes place is a major issue in disease development, epigenetics has the real potential to better explain how genes are involved in heart disease development.
The aim of my research program is thus to understand how changes in gene reading speed through epigenetic modifications is related to the development of obesity, diabetes and ultimately heart disease.
On the one hand, I study newborns and children born from pregnancies complicated by maternal obesity and diabetes because these offspring are at higher risk to have obesity and diabetes themselves later in life. On the other hand, I target HDL-cholesterol epigenetic structure components (the microRNAs) because they might reveal why cholesterol in HDL is in fact good and protects from heart diseases. The reading speed of all known human genes will be measured in thousands of people at high risk of heart disease using state-of-the-art technologies and laboratory testing.
The anticipated results of this research program will contribute to a better understanding of how epigenetics influences the long-term risk for obesity, diabetes and heart disease. They will constitute a solid basis for the improvement of prevention, care and eventually the health of affected people.