Role of fibrin biofilm and clot network architecture in thrombus stability (renewal)

Blood clots that block arteries or break loose and travel to the lungs or brain are held together by a mesh of fibrin—a protein that forms both the clot’s internal scaffold and a biofilm coating around it. This project will determine how the precise molecular arrangement of that fibrin network and its biofilm shell determines whether a clot stays put, breaks apart harmlessly, or fragments into dangerous emboli. Current treatments for thrombosis—anti-clotting drugs—carry a serious trade-off: they prevent new clots but also raise the risk of dangerous bleeding. The problem is that doctors cannot yet predict which clots will stay stable and which will break loose. This research aims to map the physical and molecular rules that govern clot stability, from the way fibrin strands are packed together to how flow and surface chemistry trigger biofilm formation. If successful, the work could lead to new diagnostic tests that distinguish stable from unstable clots, and to therapies that selectively target the clot’s structural weak points without disabling the body’s normal clotting response. That would mean fewer strokes and pulmonary emboli without the current penalty of increased bleeding risk.