Abstract
Prostacyclin (PGI2) is one of the important vascular prostanoids, the effects of which counteract those of thromboxane (TXA2), and these 2 prostanoids provide an important balance in cardiovascular homeostasis. The clinical experience of COX-2 selective inhibitors having unexpected adverse effects in patients with cardiovascular risk has opened up a debate about the role of COX-2-derived prostanoids in vascular pathophysiology. PGI2 is a major anti-atherogenic prostanoid produced by COX-2 in vascular cells, including endothelial and vascular smooth muscle cells. The balance between COX-2-derived PGI2, COX-1-derived TXA2, and other COX-2-mediated atherogenic prostanoids is a crucial factor in determining pathophysiological outcomes. Recent studies using stable PGI2 analogs and genetically deficient mice have revealed novel effects of PGI2 on its target cells, such as endothelial and endothelial progenitor cells. The role PGI2 in the physiology and pathophysiology of vascular diseases is reviewed and the recent findings linking PGI2, COX-2 and atherothrombosis are summarized.
