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Thromboxane A₂ synthase (TXAS) converts prostaglandin H2 to thromboxane A₂ (TXA₂) and has been implicated in cardiovascular disease. Will it be beneficial for cardiovascular disease in TXAS-deleted mice?

Platelet activation and aggregation is a self-amplifying process to promote quick clotting preventing uncontrolled bleeding. Upon activation, platelets secrete thromboxane A₂ (TXA₂) and ADP to activate surrounding platelets to promote thrombosis. TXA₂ is a potent platelet activator and vasoconstrictor, and its dysregulated signaling is closely linked to pathological thrombosis and vascular dysfunction. Clinically, low-dose aspirin has been widely used to inhibit TXA₂ production that is closely associated with a reduced incidence of thrombotic and cardiac events in patients with cardiovascular disease. Dysregulated platelet aggregation is associated with many diseases, such as atherosclerosis, myocardial infarction, stroke, peripheral artery disease and deep vein thrombosis.

Although reducing or inhibiting TXA₂ production is generally beneficial, we used TXAS knockout mice to investigate its role in cardiovascular disease and obtained unexpected results. Our findings may help explain the increased incidence of cardiovascular events observed in patients undergoing long-term, high-dose aspirin or NSAID therapy.