Cardiac fibroblasts as a target to limit ventricular remodelling and heart failure
The various phenotypic changes that accompany the left ventricular (LV) response to myocardial infarction are a phenomenon referred to as LV remodelling. Remodelling is supported by progressive cellular and molecular changes, eventually resulting in altered myocardial functional properties and heart failure. Our laboratory is particularly interested in the role of cardiac fibroblasts in this adverse process. We aim at further substantiating their role in the pathogenesis of LV remodelling and more particularly at identifying new potential intracellular therapeutic targets. These aims are carried out through the use of human cardiac fibroblasts in culture, mouse models of myocardial infarction or hypertrophy as well as human models of LV remodelling. The experimental approach involves various techniques of biochemistry, cellular and molecular biology (cell culture, expression and phosphorylation of proteins, enzyme assays, FACS, immunohistology immunocytology, PCR and qRT-PCR, microarray analysis).