tromboxaan

Thromboxane A2, commonly abbreviated TXA2, is a potent eicosanoid produced primarily by activated platelets. It belongs to the prostanoid family and is derived from arachidonic acid through the action of cyclooxygenase and thromboxane synthase. Because TXA2 is chemically unstable, it rapidly hydrolyzes to TXB2, which is often measured as a surrogate for TXA2 production in plasma or urine.

Biosynthesis occurs when platelets are activated and phospholipases release arachidonic acid from membrane phospholipids. Cyclooxygenase-1 converts arachidonic acid to prostaglandin H2, which thromboxane synthase then converts to TXA2. The short half-life of TXA2 means it acts locally at sites of release and is quickly inactivated, with TXB2 serving as a more stable indicator of TXA2 formation.

TXA2 exerts its effects by binding to the thromboxane receptor (TP) on platelets and on vascular smooth muscle. In platelets, TP receptor activation promotes shape change, granule release, and aggregation, reinforcing clot formation. In vascular smooth muscle, TXA2 induces vasoconstriction. The combined actions support hemostasis but can also contribute to pathological thrombosis and vasospasm when TXA2 activity is excessive.

Clinical relevance includes the role of TXA2 in cardiovascular disease. Aspirin therapeutically inhibits COX-1 in platelets, reducing TXA2 production and lowering thrombotic risk. Other NSAIDs can interfere with aspirin’s antiplatelet effect when used concomitantly. TXA2 and its stable metabolite TXB2 are used as biomarkers of platelet activation in research and clinical settings.