12:00 AM
Apr 22, 2002
 |  BioCentury  |  Tools & Techniques

Getting to the heart of COX-2 risk

COX-2 inhibitors were designed to provide relief from inflammatory pain similar to the non-steroidal anti-inflammatory drugs without the gastrointestinal toxicity associated with NSAIDs. But studies have suggested that there may be an increased risk of cardiovascular thrombotic events in people taking the inhibitors. Now researchers have published a proposed mechanism that could be responsible for increased cardiovascular risk.

Prostaglandin H2 (PGH2) is produced in cells by the cyclooxygenase enzymes. In vascular endothelial cells, the primary isoform present is COX-2, while in platelets and gastric epithelial cells, the primary isoform is COX-1.

In vascular endothelial cells, prostacyclin synthase produces prostacyclin (PGI2) from PHG2. PGI2 has vasodilatory activity and inhibits platelet clumping. In contrast, PHG2 in platelets is used by thromboxane synthase to make thromboxane A2 (TXA2), which has vasoconstrictive...

Read the full 632 word article

User Sign in

Trial Subscription

Get a 4-week free trial subscription to BioCentury

Article Purchase

$150 USD
More Info >