Antiplatelet therapy: targeting the TxA2 pathway

J Cardiovasc Transl Res. 2014 Feb;7(1):29-38. doi: 10.1007/s12265-013-9529-1. Epub 2013 Dec 19.


The thromboxane (Tx) A2 pathway is a major contributor to the amplification of the initial platelet activation process. TxA2 mediates its effect through the thromboxane prostanoid (TP) receptor that is expressed not only in platelets, but also in endothelial cells, macrophages, and monocytes, and thus contributes to the development of atherosclerotic lesions. The TxA2 pathway is therefore a major target in the treatment of cardiovascular disease. Aspirin-the most widely used antiplatelet drug-is very effective at inhibiting platelet-derived TxA2 synthesis. However, aspirin's effects can be overcome by several other soluble agonists such as isoprostanes, which are aspirin-insensitive ligands of the TP receptor that are preferentially produced in diabetes mellitus. Other drugs, with either inhibitory effects on Tx synthase or antagonist effects on TP, have been developed with the hope of providing a better, more complete inhibition of the TxA2 pathway.

Publication types

  • Review

MeSH terms

  • Animals
  • Atherosclerosis / blood
  • Atherosclerosis / drug therapy*
  • Blood Platelets / drug effects*
  • Blood Platelets / metabolism
  • Drug Design
  • Enzyme Inhibitors / therapeutic use
  • Humans
  • Molecular Targeted Therapy*
  • Platelet Activation / drug effects*
  • Platelet Aggregation Inhibitors / therapeutic use*
  • Receptors, Thromboxane A2, Prostaglandin H2 / antagonists & inhibitors
  • Receptors, Thromboxane A2, Prostaglandin H2 / metabolism
  • Signal Transduction / drug effects*
  • Thromboxane A2 / metabolism*
  • Thromboxane-A Synthase / antagonists & inhibitors
  • Thromboxane-A Synthase / metabolism


  • Enzyme Inhibitors
  • Platelet Aggregation Inhibitors
  • Receptors, Thromboxane A2, Prostaglandin H2
  • Thromboxane A2
  • Thromboxane-A Synthase