Traditionally, venous thrombosis has been seen as the consequence of a regulated cascade of proteolytic steps leading to the polymerization of fibrinogen and fibrin crosslinking that is facilitated by platelets. A new view of thrombosis is providing a more integrated concept, with components of the vascular wall contributing to the vascular remodeling of thrombosis. Angiogenesis and inflammation are two key mechanisms that safeguard venous thrombus resolution and restitution of vascular patency after thrombosis. Disturbance of these processes leads to thrombus persistence and has potentially severe consequences for affected patients. Examples for clinical conditions associated with recurrent or persisting venous thrombosis are post-thrombotic syndrome or chronic thromboembolic pulmonary hypertension. Recently, studies using animal models of venous thrombosis have contributed to a better understanding of thrombus non-resolution that will eventually lead to modification of current treatment concepts. For example, recent data suggest that innate immunity is involved in the modification of thrombosis.
Keywords: angiogenesis; fibrosis; inflammation; thrombosis; thrombus resolution.