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Cyclooxygenase-2 and inflammation in atherosclerosis
MacRae F Linton1, Sergio Fazio
1Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. macrae.linton@vanderbilt.edu
Current Opinion in Pharmacology
|April 6, 2004
Summary
Cyclooxygenase-2 (COX-2) plays a role in inflammation and atherosclerosis. Inhibiting COX-2 may reduce early atherosclerosis, but its impact on advanced lesions and cardiovascular events requires further study.
Area of Science:
- Biomedical Science
- Inflammation Research
- Cardiovascular Biology
Background:
- Cyclooxygenase (COX) regulates eicosanoids involved in atherosclerosis and thrombosis.
- COX-2, a key inflammatory mediator, is upregulated in macrophages and implicated in atherogenesis.
- Macrophage COX-2 is downregulated by oxidized LDL and liver X receptors, linking cholesterol and inflammation.
Purpose of the Study:
- To investigate the role of COX-2 in atherogenesis.
- To evaluate the impact of COX-2 inhibition on cardiovascular events.
Main Methods:
- Studies in mouse models of atherosclerosis.
- Analysis of COX-2 regulation by oxidized LDL and liver X receptors.
- Meta-analyses of randomized trials on COX-2 inhibitors.
Main Results:
- Selective COX-2 inhibition or deletion in macrophages protects against early atherosclerosis in mice.
- Macrophage COX-2 expression may be attenuated in advanced lesions.
- Meta-analyses have not shown excess cardiovascular events with COX-2 inhibitors.
Conclusions:
- COX-2 inhibition shows potential for reducing early atherosclerosis via anti-inflammatory effects.
- The role of macrophage COX-2 in advanced lesions warrants further investigation.
- Prospective studies are needed to confirm the cardiovascular safety of selective COX-2 inhibitors.