Journal
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 25, Issue 4, Pages 679-685Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.ATV.0000157899.35660.61
Keywords
aspirin; C/EBP; COX-2; inflammation; NF-kappa B
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Funding
- NHLBI NIH HHS [R01 HL-50675] Funding Source: Medline
- NINDS NIH HHS [P50 NS-23327] Funding Source: Medline
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Cyclooxygenase-2 (COX-2) is a highly inducible enzyme exerting diverse actions on cell functions, including proliferation, migration, and DNA damage. Enhanced COX-2 expression may be protective, but excessive expression may be harmful, causing inflammation, atheromatous plaque instability, and intimal hyperplasia. COX-2 transcriptional activation by proinflammatory mediators has been extensively characterized. In this review, the role of C/EBP in regulating COX- 2 transcription is highlighted. Recent advances in control of COX- 2 transcription by aspirin and salicylate and by a cell cycle - dependent endogenous mechanism are described. The recent progress sheds light on the pathophysiological mechanisms of COX- 2 and new transcription-based strategy for controlling COX- 2 overexpression and COX- 2 - mediated cardiovascular diseases.
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