PT  - JOURNAL ARTICLE
AU  - Burkhard Hinz
AU  - Kay Brune
TI  - Cyclooxygenase-2—10 Years Later
AID  - 10.1124/jpet.300.2.367
DP  - 2002 Feb 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 367--375
VI  - 300
IP  - 2
4099  - http://jpet.aspetjournals.org/content/300/2/367.short
4100  - http://jpet.aspetjournals.org/content/300/2/367.full
SO  - J Pharmacol Exp Ther2002 Feb 01; 300
AB  - The enzyme cyclooxygenase (COX) catalyzes the first step of the synthesis of prostanoids. In the early 1990s, COX was demonstrated to exist as two distinct isoforms. COX-1 is constitutively expressed as a “housekeeping” enzyme in most tissues. By contrast, COX-2 can be up-regulated by various pro-inflammatory agents, including lipopolysaccharide, cytokines, and growth factors. Whereas many of the side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) (e.g., gastrointestinal ulceration and bleeding, platelet dysfunctions) are caused by a suppression of COX-1 activity, inhibition of COX-2-derived prostanoids facilitates the anti-inflammatory, analgesic, and antipyretic effects of NSAIDs. During the past few years specific inhibitors of the COX-2 enzyme have emerged as important pharmacological tools for treatment of pain and arthritis. However, although COX-2 was initially regarded as a source of pathological prostanoids only, recent studies have indicated that this isoenzyme mediates a variety of physiological responses within the organism. The present review assesses recent advances in COX-2 research, with particular emphasis on new insights into pathophysiological and physiological functions of this isoenzyme. The American Society for Pharmacology and Experimental Therapeutics