Mouse Models, Risk Factors, and Treatments of Venous Thrombosis

Abstract

Deep vein thrombosis and pulmonary embolism are collectively called venous thromboembolism (VTE) and are a major cause of morbidity and mortality in the United States and Europe. March is deep vein thrombosis awareness month in the United States, and each year Arteriosclerosis, Thrombosis, and Vascular Biology marks this event with a series of reviews on VTE. This year we have 3 excellent articles on (1) mouse models of venous thrombosis, (2) risk factors for VTE in humans, and (3) the new generation of oral anticoagulants that are available to treat VTE. See accompanying articles on pages 556, 563, and 569 The first review, by Diaz et al1 describes how the use of mouse models has increased our understanding of the mechanisms of initiation, propagation, and resolution of venous clots. The obvious advantage of mice is that we can determine the effect of the loss or mutation of any given gene on thrombosis. Indeed, work with P-selectin knockout mice suggested a role for P-selectin in venous thrombosis that was subsequently confirmed in nonhuman primates. It will be interesting to see whether P-selectin inhibitors will be successfully developed as anticoagulant drugs. Mice have several disadvantages, however, including their small size, their resistance to thrombosis, and the surgical challenges of working with small vessels. Diaz et al1 evaluate 4 inferior vena cava (IVC) thrombosis models. The ferric chloride model induces oxidative damage to the vessel wall that produces an occlusive thrombosis. The advantage of this model is that it is …