Heart failure is one of the leading causes of death worldwide. Current therapeutic strategies are inefficient and cannot cure this chronic and debilitating condition. Ultimately, heart transplants are required for patient survival, but donor organs are scarce in availability and only prolong the lifespan of patients for a limited time. Fibrosis is one of the main pathological features of heart failure, caused by inappropriate stimulation of fibroblasts and excessive extracellular matrix production. Furthermore, it is estimated that about 45% of all diseases include fibrosis as a pathological feature. Therefore, an in-depth understanding of the fibroblast is essential to underpin effective therapeutic treatments for heart failure and other fibrotic diseases.
Following on our previous findings that fibroblasts isolated from the heart display a cardiogenic identity, we are expanding our studies to: 1. understand the role of the cardiogenic network identified by us in heart development, homeostasis and disease; 2. generate new murine genetic tools to study fibroblast biology and 3. identify tissue-specific properties of fibroblasts for organ-specific anti-fibrotic treatments.