PhD position Heart-on-a-Chip: in-vitro Cardiac Fibrosis Modelling and Beyond

Cardiovascular disease is the leading cause of deaths worldwide. In the US, heart diseases account for nearly 800,000 of deaths per year. Most heart disease cases involve cardiac fibrosis characterized by excessive deposition of extracellular matrix (ECM) proteins by myofibroblasts, which are activated form of cardiac fibroblasts (CFs). It causes stiffening of the heart wall (myocardium), which reduces pumping capability of the heart and accelerates the progression to heart failure. However, the CF as a cell type and the pathological development of fibrosis are still poorly understood. As a result, there are currently limited clinical interventions that effectively target CF and its pathological contributions to disease progression. One key change that lead to cardiac fibrosis is the upregulation of α‐smooth muscle actin (aSMA) expression, a contractile protein, by activated myofibroblasts. This event coexists with the increase of stiffness and structure of myocardium, loss of contraction and pumping capability of the heart.