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Cyclooxygenase‐dependent signalling: molecular events and consequences
Author(s) -
Versteeg Henri H,
van Bergen en Henegouwen Paul M.P,
van Deventer Sander J.H,
Peppelenbosch Maikel P
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00105-2
Subject(s) - prostanoid , cyclooxygenase , signal transduction , heterotrimeric g protein , receptor , receptor tyrosine kinase , microbiology and biotechnology , g protein , inflammation , chemistry , thromboxanes , pharmacology , biology , enzyme , biochemistry , immunology , arachidonic acid
Non‐steroidal anti‐inflammatory drugs (NSAIDs) currently attract large interest. Next to pain relief, NSAIDs have important anti‐thrombotic and anti‐oncogenic effects. NSAIDs exert their action by inhibition of cyclooxygenase, the enzyme responsible for the production of prostanoids. Prostanoid signal transduction is still poorly understood, but it has become clear that these inflammatory lipids influence cellular physiology at three different levels: (1) activation of a 7× transmembrane receptor coupled to heterotrimeric G proteins, (2) the inhibition of inflammation by activating corticosteroid‐like receptors, (3) participation in receptor protein tyrosine kinase signal transduction. In this review prostanoid signalling at these three different levels will be reviewed and the relevance in (patho)physiological processes will be evaluated.