Protease-activated receptors in vascular smooth muscle cells: a bridge between coagulation and vascular remodeling

This thesis explores how the body’s natural repair system, coagulation, not only stops bleeding but also sends signals to blood vessel cells. Sometimes, these signals can be harmful. Central to this process are protease-activated receptors (PARs) - tiny “doorbells” on cells that respond to coagulation factors. One important group of cells affected are vascular smooth muscle cells (VSMCs). Normally, VSMCs help keep blood vessels stable, but when they receive the wrong signals, they change behavior and start reshaping the vessel wall. This remodeling makes vessels stiffer, narrower, and more prone to cardiovascular disease. This thesis investigates how different PARs drive these harmful changes and examines how current drugs, such as rivaroxaban, may protect blood vessels. Overall, the findings highlight new pathways that could be targeted to prevent or slow down cardiovascular disease, offering fresh perspectives for future treatments.