Heart failure occurs when the heart loses the ability to pump sufficient blood to metabolising tissues, and is the leading cause of death in today’s society. The most common contributing factor of heart failure is cardiac fibrosis, which arises from most cardiovascular pathologies including myocardial infarction (heart attack) and hypertension (high blood pressure). For a pathology that carries such clinical significance, the mechanisms behind cardiac fibrosis are poorly understood. Here, we aim to investigate how engineered nanovesicles can be used to deliver cytoprotectives to fibrotic cardiac tissue.
This project will employ animal models of cardiac fibrosis, and the use of mass spectrometry to understand specific molecular and cellular repair processes through changes in proteome and phosphoproteome landscape. Such knowledge will help define approaches to temporally regulate the progression of cardiac fibrosis.