Our laboratory studies disease mechanisms in venous thrombosis with a major area of focus on regulation of venous homeostasis. We are exploring endogenous vasculo-protective enzymes that function at the intersection of inflammation and coagulation. We are also interested in disease pathways that are triggered by abnormal innate immune activation and cell stress responses that lead to an imbalance in coagulation and fibrinolysis. Our work utilizes human vascular cells and tissues from patients with vascular disease, primary cultures endothelial cells, and mouse models of venous thrombosis.


Veins are the most commonly used conduit to surgically bypass arterial stenoses. Veins are structurally distinct from arteries, and are forced to adapt to the arterial environment when used as arterial bypass grafts. Unfortunately, this remodeling can be pathologic and a high proportion of vein bypass grafts will fail, leading to ischemia or additional procedures. We are specifically studying the effect of extracellular nucleotide signalling in vein graft maladaptation. Using state-of-the-art mechanical stretch models that mimic vein graft function and mouse models of vein graft disease, our investigative efforts have focused on venous adaptations to arterial environments.

Funding sources

National Institutes of Health

National Heart, Lung & Blood Institute

American Venous Forum Foundation-JOBST

Bo Schembechler Heart of A Champion Foundation

University of Michigan Frankel Cardiovascular Center

McKay Foundation