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Antiplatelet therapy: targeting the TxA2 pathway.
Journal article

Antiplatelet therapy: targeting the TxA2 pathway.

  • Fontana P Division of Angiology and Haemostasis, Faculty of Medicine and University Hospitals of Geneva, 4, rue Gabrielle-Perret-Gentil, 1211, Geneva, Switzerland, pierre.fontana@hcuge.ch.
  • Zufferey A
  • Daali Y
  • Reny JL
  • 2013-12-20
Published in:
  • Journal of cardiovascular translational research. - 2014
Animals
Atherosclerosis
Blood Platelets
Drug Design
Enzyme Inhibitors
Humans
Molecular Targeted Therapy
Platelet Activation
Platelet Aggregation Inhibitors
Receptors, Thromboxane A2, Prostaglandin H2
Signal Transduction
Thromboxane A2
Thromboxane-A Synthase
English 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.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://folia.unifr.ch/global/documents/108702
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