Cyclooxygenase-2 expression and function in renal pathophysiology.
Cyclooxygenase (COX) constitutes the rate-limiting enzyme in the biosynthetic cascade of prostaglandin (PG). Evidence has accrued suggesting pathophysiological states with altered COX-2 activity and expression. Recent experimental evidence suggests that COX-2 has a pathogenetic role in some of these derangements. In other situations, the effect of altered COX-2 regulation is unclear or possibly beneficial. These processes suggest new areas for potential use of COX-2-specific inhibitors. Conversely, in some conditions COX-2-specific inhibitors should be avoided. The conventional view is that COX-2 is an inducible enzyme. However, COX-2 is also active in the constitutive production of prostanoids in the kidney. Consequently, the pathophysiological states discussed herein include not only COX-2 induction during inflammation but also derangements in COX-2 expression and function caused by non-inflammatory stimuli.
Komers
Radko
R
Division of Nephrology and Hypertension, Oregon Health Sciences University, Portland, Oregon, USA.
Epstein
Murray
M
D000818:Animals; D051546:Cyclooxygenase 2; D005923:Glomerulosclerosis, Focal Segmental / Q000201:enzymology; D006801:Humans; D006978:Hypertension, Renovascular / Q000201:enzymology; D007527:Isoenzymes / Q000378:metabolism*; D007674:Kidney Diseases / Q000201:enzymology*; D008565:Membrane Proteins; D009393:Nephritis / Q000201:enzymology; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
D007527:Isoenzymes; D008565:Membrane Proteins; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases