Project B05

Cardiac injury commonly triggers profibrotic responses that drive excessive ECM deposition and increase tissue stiffness. This project will define how ECM secretion and stiffness shape pericyte and endothelial responses to cardiac damage. We will examine stiffness-dependent secretion of YBX1 and LAP3 in vivo and in vitro and characterize their molecular mechanisms. Finally, we will test whether approved anti-fibrotic drugs can be repurposed to target myocardial stiffness, reduce vascular dysfunction, and improve the cardiac response to injury.