Research News

Disulfide HMGB1 derived from platelets coordinates venous thrombosis in mice

Deep venous thrombosis (DVT) is one of the most common cardiovascular diseases, but its pathophysiology remains incompletely understood. Although sterile inflammation has recently been shown to boost coagulation during DVT, the underlying molecular mechanisms are not fully resolved, which could potentially identify new anti-inflammatory approaches to prophylaxis and therapy of DVT. Using a mouse model of venous thrombosis induced by flow reduction in the vena cava inferior, we identified blood-derived high-mobility group box 1 protein (HMGB1), a prototypical mediator of sterile inflammation, to be a master regulator of the prothrombotic cascade involving platelets and myeloid leukocytes fostering occlusive DVT formation. [mehr...]

Oral thrombin inhibitor aggravates platelet adhesion and aggregation during arterial thrombosis

The hidden side of an anticoagulant

For patients with atrial fibrillation and other conditions that predispose them to thrombosis, long-term anticoagulation treatment is the norm. Surprisingly, oral thrombin inhibitors, one of the types of anticoagulants used in humans, slightly increased the risk of acute coronary syndromes in clinical studies. To understand this apparent paradox, Petzold et al. compared the effects of treatment with oral thrombin inhibitors, treatment with vitamin K antagonists (another class of anticoagulants), or no treatment at all in patients’ blood and in mouse models of arterial thrombosis, confirming the observations from clinical studies and identifying some of the underlying mechanisms: [mehr...]