Credentials: MBBS, PhD
Position title: Assistant Professor of Medicine
Our laboratory studies the interactions between metabolism and blood clot lysis. Fibrinolysis, the primary mechanism that dissolves a blood clot, is initiated by a serine protease tissue-type plasminogen activator (tPA). Our previous study discussed a novel source and regulation of endogenous basal plasma tPA derived from hepatocytes, which is important for fibrinolysis when a vessel injury occurs. The tPA activity is inhibited primarily by the serpin plasminogen activator inhibitor 1 (PAI-1). A balance between tPA and PAI-1 in plasma is essential for preventing excessive clotting. Our recent study revealed the mechanism of how hepatocytes sense metabolic stresses and imbalance the production of tPA and PAI-1, influencing the degree of impaired fibrinolysis in obesity. The goal of our laboratory is to understand the role of hepatocyte-derived tPA and basal fibrinolysis in hemostasis, and to develop diagnostic/ preventive/ therapeutic strategies that can be used to combat atherosclerosis, thrombosis, and bleeding disorders. Specific areas of research interests include: 1) a new link between reduced fibrinolysis and dyslipidemia, 2) circadian regulation of basal fibrinolysis and the morning onset of thrombotic events, 3) the role of hepatocyte tPA and liver injuries, 4) increased fibrinolysis in hemophilia, and 5) a timely study of fibrinolysis in COVID- 19. As many of these processes are dysregulated in obesity, insulin resistance and diabetes, my research program is well-aligned with the mission of the Wisconsin Diabetes Research Center.