Prostaglandins play important roles in the pathophysiological mechanism of action of platelets and endothelial cells in the cardiovascular system. The two isoforms of cyclo-oxygenase, respectively cyclo-oxygenase-1 and cyclo-oxygenase-2, are differently expressed in these cells. Activated platelets show a relatively large amount of cyclo-oxygenase-1, whereas endothelial cells have the gene for cyclo-oxygenase-2, the expression of which follows cell activation. In the atherosclerosis lesion, prostaglandin synthesis is mainly mediated by the inducible cyclo-oxygenase-2 expressed in macrophages/foam cells, smooth muscle cells and endothelial cells. Aspirin, a selective platelet cyclo-oxygenase-1 inhibitor, still remains the most extensively studied antiplatelet agent, even though there is growing evidence that many other compounds could be valuable either in association, or alternatives in antithrombotic therapy.
- Endothelial cells
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