thrombaxane

Thrombaxane, more correctly thromboxane A2 (TXA2), is a potent eicosanoid derived from arachidonic acid. It is produced primarily by activated platelets and serves as a key mediator of hemostasis and thrombosis. TXA2 is short-lived and rapidly degrades to thromboxane B2 (TXB2), which is often measured as an indicator of TXA2 production.

Biosynthesis occurs when phospholipase A2 releases arachidonic acid from membrane phospholipids. Cyclooxygenase-1 (COX-1) converts arachidonic acid to the intermediate prostaglandin G2/H2, and thromboxane synthase then forms TXA2. Because TXA2 is highly unstable, it acts locally and briefly before forming TXB2.

The primary actions of TXA2 are vasoconstriction and the promotion of platelet aggregation. Through the thromboxane receptor (TP), TXA2 causes smooth muscle contraction and enhances platelet activation, contributing to plug formation at sites of vascular injury. It can also provoke bronchoconstriction in susceptible individuals and modulate vascular tone.

Physiologically, TXA2 supports rapid hemostasis after endothelial injury. Pathologically, excessive TXA2 activity can contribute to thrombosis and cardiovascular risk. Therapies that blunt TXA2 signaling, notably aspirin, inhibit COX-1 in platelets and reduce TXA2 production, providing an antiplatelet effect. Endothelial cells produce prostacyclin (PGI2), which opposes TXA2 actions by inhibiting platelet aggregation and causing vasodilation, helping to balance hemostasis.

Measurement of TXA2 is typically inferred from TXB2 levels in serum or urine, given TXA2’s instability.