The roles of prostacyclin (PGI2) and thromboxane (TxA2) in the pathogenesis of cardiovascular disease have been debated for more than 30 years. Cheng et al. (see the Perspective by Vane) show that PGI2 modulates platelet-vascular interactions in vivo and limits the deleterious vascular proliferative response to TxA2. In contrast to aspirin, which suppresses both PGI2 and TxA2, the recently introduced cyclooxygenase-2 (COX-2) inhibitors suppress PGI2 only. The interplay between PGI2 and TxA2 could be the molecular basis of the cardiovascular complications that have been seen in some patients who have substituted COX-2 inhibitors for aspirin.
Y. Cheng, S. C. Austin, B. Rocca, B. H. Koller, T. M. Coffman, T. Grosser, J. A. Lawson, G. A. FitzGerald, Role of prostacyclin in the cardiovascular response to thromboxane A2. Science 296, 539-541 (2002). [Abstract] [Full Text]