The ability to regenerate the heart is lost with evolution, with the transition to a closed high pressure circulatory system and a four-chambered heart made of highly specialized and differentiated contractile cells. In adult mammalians hearts, in response to an injury such as myocardial infarction, the necrotic tissue is replaced by a non-contractile fibrotic scar. The formation of a scar is a relatively more rapid repair mechanism which can prevent cardiac rupture, but an extensive scar and excessive fibrosis lead to adverse remodeling and chronic cardiac failure, one of the leading cause of mortality and morbidity worldwide.
We are interested in studying the mechanisms involved in scar formation, and the dynamic changes in cardiac interstitial populations in response to injury, in order to tune them for a better cardiac repair and remodeling. Cardiac fibroblasts play a crucial role in this process, thus we aim to identify tissue-specific properties of fibroblasts for organ-specific anti-fibrotic treatments.