Inducible COX-2 dominates over COX-1 in prostacyclin biosynthesis: Mechanisms of COX-2 inhibitor risk to heart disease

COX-2 inhibitor.

he developed severe psoriasis responsive only to repeated courses of the then newly available PUVA (psoralen plus UVA radiation) therapy. Between 1973 and 1993 he received PUVA once a week. During treatment no genital protection was used although he had never received UV therapy directly to the genital area. Two years after the onset of psoriasis he developed peripheral inflammatory arthritis. ...

COX-2, the dominant source of prostacyclin.

COX-1 and COX-2 products in the gut: therapeutic impact of COX-2 inhibitors.

Despite the considerable range of newly identified disease modifying approaches to the control of the inflammatory process reported over the past 10–20 years, only a few have yet gained widespread clinical acceptance. In contrast, the very recent advent of the class of anti-inflammatory agents termed COX-2 selective inhibitors is already having a significant impact on current clinical prescribi...

COX-2-derived prostacyclin modulates vascular remodeling.

Suppression of prostacyclin (PGI2) biosynthesis may explain the increased incidence of myocardial infarction and stroke which has been observed in placebo controlled trials of cyclooxygenase (COX)-2 inhibitors. Herein, we examine if COX-2-derived PGI2 might condition the response of the vasculature to sustained physiologic stress in experimental models that retain endothelial integrity. Deletio...

COX-2 in cardiovascular disease.

Prostanoids are a large family of lipid mediators derived from the arachidonic acid metabolites of the cyclooxygenase (COX) enzymes. Therapeutically, COX is the target of the nonsteroid antiinflammatory drugs (NSAIDs), a chemically diverse group that includes ibuprofen, naproxen, and diclofenac, among dozens of others. Inhibition of prostanoid production by traditional NSAIDs accounts for all t...