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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:956.)
© 2006 American Heart Association, Inc.

Editorials

COX-2 in Cardiovascular Disease

David Bishop-Bailey; Jane A. Mitchell; Timothy D. Warner

From Cardiac, Vascular, & Inflammation Research (D.B.-B., T.D.W.), William Harvey Research Institute, Queen Mary University of London; and Cardiothoracic Pharmacology (J.A.M.), Unit of Critical Care Medicine, National Heart and Lung Institute, Royal Brompton Hospital, Imperial College School of Medicine, London, UK.

Correspondence to Dr David Bishop-Bailey, Cardiac, Vascular, & Inflammation Research, William Harvey Research Institute, Queen Mary University of London, Charterhouse Sq, London, EC1M 6BQ UK. E-mail d.bishop-bailey@qmul.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 their major therapeutic effects, such as the dampening down of inflammation and the reduction of fever, and their potentially severe adverse side effects, most commonly within the gastrointestinal tract.^1,2

See page 1137

Since the early 1990’s it has been clear there are two distinct enzymes responsible for the production of prostanoids: a constitutive COX-1 found in all tissues and an inflammation-associated enzyme COX-2.^1,2 COX-2 is constitutively expressed in only a few sites, such as parts of the kidney and central nervous system, but is highly upregulated and active at sites of inflammation. These findings led to the hypothesis that selective COX-2 inhibitors could be antiinflammatory without the major side effects associated with traditional NSAIDs. Against this background several COX-2–selective inhibitors have been produced and brought to market, the first two being celecoxib (Celebrex) and rofecoxib (Vioxx).

Preclinical studies of these COX-2–selective inhibitors were extremely promising. In animal models, for example, they were demonstrated to be as efficacious as traditional NSAIDs but to be lacking their toxic actions on the gastrointestinal tract. Clinical trials have, however, been marred by controversy. The CLASS trial for celecoxib, a 12-month osteoarthritis study of celecoxib, demonstrated celecoxib to have improved safety . . . [Full Text of this Article]

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Victoria L. King, Darshini B. Trivedi, Jonathan M. Gitlin, and Charles D. Loftin
Arterioscler Thromb Vasc Biol 2006 26: 1137-1143. [Abstract] [Full Text] [PDF]

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