As a cardiologist and clinical vascular medicine specialist, Dr. Kanthi’s laboratory aims to understand how inflammation and coagulation contribute to vascular disease. We are interested in developing a deeper understanding of how innate immune circuits and communicate with coagulation and the vessel wall to license or restrict thrombosis.
Dr. Kanthi joined the NIH to build a translational vascular medicine research program. His team has studied the role of inlammasome activation and purine signaling in venous thrombosis (JCI, ATVB, Nature Communications). The Laboratory of Vascular Thrombosis and Inflammation (LVTI)has made seminal discoveries in COVID-19 pathology, being the first to identify neutrophil extracellular traps in patients with COVID-19 (JCI Insight), a new calprotectin biomarker for COVID-19 severity (J Leuk Biol), and the discovery of prothrombotic autoAntibodies in patients with COVID-19 (Science Translational Medicine).
With expertise in thrombo-inflammation and vascular biology, Dr. Kanthi launched a clinical trial at the University of Michigan (NCT04399179) to test dipyridamole, a repurposed FDA-approved drug in patients with COVID-19.
The goal of the LVTI is to identify the molecular and cellular processes that lead to vascular thrombo-inflammation and design better therapeutic approaches for patients with vascular disease.
Our team studies disease mechanisms in venous thrombosis with a major area of focus on regulation of venous homeostasis. We investigate endogenous molecules like the prototypical inflammasome effector interleukin-1β, and vasculo-protective purinergic enzymes at the intersection of inflammation and coagulation.
We are investigating the molecular and cellular mechanisms that contribute to COVID-19 severity. Working closely with our collaborator, Dr. Jason Knight, we were the first to describe the role of neutrophil activation and extracellular trap formation in COVID-19. Our findings have led to several clinical trials, and been validated by several groups.
Additional Coverage: Scientific American
We leverage our strengths in inflammation and thrombosis , two processes at the heart of severe COVID-19 illness to understand this disease, and develop potential new treatments. We are also interested in disease pathways that are triggered by abnormal innate immune activation and cell stress responses. Our team discovered that COVID-19 triggers the production of prothrombotic autoantibodies in blood. Our work utilizes human blood, tissues from patients with vascular disease, primary cultures endothelial cells, and mouse models of venous thrombosis.