Arterial and venous thromboses are leading causes of death and
disability worldwide. Arterial thrombi arise in vessels with high fluid
shear forces, where plaque rupture triggers the formation of platelet-
rich thrombi. In contrast, venous thrombi typically originate
in hypoxic venous valve pockets and reduced blood flow (stasis),
where activated endothelium triggers the formation of red blood
cell-rich thrombi. Decades of gross and microscopic analyses of
thrombi, combined with recent advances in mouse models, have
revealed unique mechanisms contributing to each of these types of
thrombi. Recent work in our laboratory has uncovered newly-recognized
pathologic roles for several blood components, including
fibrinogen, factor XIII, and red blood cells in thrombus formation.
Our data indicate these components contribute to arterial and venous
thrombi in unique ways. By identifying these mechanisms, our
findings have exposed new potential therapeutic targets for reducing
mortality and morbidity due to thrombosis.