Uric Acid induces a pro-atherothrombotic phenotype in human endothelial cells by imbalancing TF/TFPI pathway

Many evidences show that elevated plasma levels of uric acid (UA) are associated to the increased risk of developing athero-thrombotic cardiovascular events. Hyperuricemia is a risk factors for endothelial dysfunction (ED). ED is involved in the pathophysiology of athero-thrombosis since dysfunctional cells lose their physiological, antithrombotic properties. We have investigated whether UA might promote ED by modulating the TF/TFPI balance finally changing the antithrombotic characteristics of endothelial cells.