The team's major research interests are based on the molecular/genetic basis of responses to cardiovascular drugs and the development of new predictive tools and more personalized therapeutics for cardiometabolic diseases. We use the emerging genomics knowledge and technologies to develop innovative therapies for cardiovascular diseases. The individual projects focus on the use of genetic and genomic profiles to adapt medications and on the genomic manipulation to treat cardiovascular diseases. The global objective is to further develop new therapeutic approaches for cardiovascular diseases and especially genome-guided therapies.
The primary research activities involve cardiovascular medications. Owing to an active collaboration with the Department of Genetics and Genomic Sciences colleagues, we are using last generation technologies such as whole-exome sequencing to identify new genetic markers associated with pathways of drug action and determine whether they can be predictors of medication response and activity in the body. Following previous achievements in the description of the clopidogrel pharamacogenetics, the team’s efforts are currently directed at studies of drugs used to treat atherothrombotic diseases.
To complement these pharmacogenomics studies and to provide new mechanistic models, we are also investigating the potential of human induced pluripotent stem cells in the field of personalized medicine. By generating patient-specific iPS derived cardiomyocytes, we aim to develop 2D- and 3D- in vitro models that are based on human cardiac tissue and could be used to identify effective drug treatments and to predict side effects that may only appear in a small subset of patients.
The second research axis is to identify new drug targets for cardiovascular diseases. We have discovered a new source of calcium entry in cardiomyocyte that occurs in the early stages of cardiac remodeling. By using a combination of RNA interference and gene transfer, we are studying the functional consequences of modulating this regulator hypertrophic and heart failure models.