Source:http://linkedlifedata.com/resource/pubmed/id/10225537
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1999-6-14
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pubmed:abstractText |
The existence of two distinct isoforms of cyclooxygenase (COX), which convert arachidonic acid to prostanoids, is now well established. COX-1, which is constitutively expressed in many tissues (including the gastrointestinal tract, platelets, and kidney) is responsible for producing prostanoids that regulate normal housekeeping or physiologic functions. In contrast, COX-2 is the inducible form responsible for the production of prostanoids in response to a variety of evoking stimuli in different tissues and for mediation of inflammation and pain in certain diseases. Since the identification of COX-2, a great deal of research has been devoted to elucidating and understanding its molecular and physiologic characteristics. As a result of research into the differences between COX-1 and COX-2, new insights into the role of each isoform in normal homeostasis and in their responses to exogenous stimuli have emerged. Besides its induction in cells at inflammatory sites, COX-2 is known to be induced in the kidney in response to sodium depletion or in hyperfiltration states; in postsynaptic excitatory neurons in the brain after electroconvulsive stimulation, in the ovary and uterus during ovulation and implantation; in intestinal epithelium after bacterial infection; as well as in colon adenoma and carcinoma cells. These findings, largely from animal studies, have suggested a broader spectrum of biologic activity of COX-2 and potential alterations of specific physiologic or protective mechanisms by inhibition of COX-2, as well as potential new clinical targets of therapy with COX-2 inhibitors. As COX-2 appears to play an important role in pathologic processes other than pain and inflammation, ongoing research is investigating the potential utility of COX-2 inhibitors in other conditions, such as colonic polyposis, colorectal cancer, and Alzheimer's disease.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PTGS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0380-0903
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
56
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
25-30
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:10225537-Animals,
pubmed-meshheading:10225537-Arthritis,
pubmed-meshheading:10225537-Colorectal Neoplasms,
pubmed-meshheading:10225537-Cyclooxygenase 2,
pubmed-meshheading:10225537-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:10225537-Cyclooxygenase Inhibitors,
pubmed-meshheading:10225537-Humans,
pubmed-meshheading:10225537-Isoenzymes,
pubmed-meshheading:10225537-Membrane Proteins,
pubmed-meshheading:10225537-Prostaglandin-Endoperoxide Synthases,
pubmed-meshheading:10225537-Research
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pubmed:year |
1999
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pubmed:articleTitle |
Specific COX-2 inhibitors in arthritis, oncology, and beyond: where is the science headed?
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pubmed:affiliation |
Department of Internal Medicine, The University of Texas Southwestern Medical Center at Dallas, 75235-8884, USA.
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pubmed:publicationType |
Journal Article,
Review
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