Cyclooxygenase‐dependent signalling: molecular events and consequences

FEBS Letters - Tập 445 - Trang 1-5 - 1999
Henri H Versteeg1,2, Paul M.P van Bergen en Henegouwen2, Sander J.H van Deventer1, Maikel P Peppelenbosch1
1Laboratory for Experimental Internal Medicine, Academic Medical Centre, G2-130, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
2Department of Molecular Cell Biology, Institute for Biomembranes and Lipid Biology, Utrecht University, Padualaan 8, Utrecht, The Netherlands

Tóm tắt

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.


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