The number of deaths that are attributable to pulmonary embolism resulting from deep vein thrombosis (DVT) in the UK (> 25 000/year) is greater than the number caused by breast cancer, HIV, and road traffic-accidents combined [1]. Approximately one third of patients with DVT develop post-thrombotic syndrome, which is characterised by long-term and debilitating symptoms including leg pain, swelling, and ulceration [2]. Post-thrombotic complications are not, however, a corollary of DVT, as clinical studies show that rapid resolution improves patient outcome and reduces post-thrombotic complications [3-5]. Current treatments for DVT include anticoagulation and thrombolysis. Anticoagulants prevent thrombus extension, but do little to remove the thrombus, which naturally resolves through a slow process of organisation similar to wound healing [6]. Thrombolysis removes the thrombus rapidly, but its use is restricted to fresh thrombus, and furthermore, both anticoagulation and thrombolysis predispose to an increased risk of pathological bleeding. Novel therapies that accelerate thrombus resolution without the risk of haemorrhage may arise from a better understanding of the molecular and cellular mechanisms that control this remodelling process.
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