Cyclooxygenase-2 inhibition: vascular inflammation and cardiovascular risk
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Updated: Aug 9, 2026

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats
Published on: December 5, 2017
Francesco Cipollone1, Maria Luigia Fazia
1Centro Regionale per la Prevenzione dell'Aterosclerosi, Via Colle dell'Ara, 66013 Chieti, Italy. fcipollone@unich.it
Abstract:
The inducible isoform of cyclooxygenase-2 (COX-2) plays a role in pathophysiologic processes like inflammation and pain but is also constitutively expressed in tissues such as the kidney or vascular endothelium, where it exerts important physiologic functions. Although much evidence exists that implicates COX-2 in atherosclerosis, its role in this setting remains substantially uncertain. This observation is also confirmed by the results of clinical trials of selective COX-2 inhibitors. Treatment with these drugs, developed with the assumption that they would be as effective as nonselective COX inhibitors but without their gastrointestinal side effects, has been reported to be associated with an increased cardiovascular risk. In this article, we review the pattern of expression of COX-2 in the cellular players of atherothrombosis, its role as a determinant of plaque vulnerability, and the vascular effects on prostanoid inhibition by COX-2 inhibitors.
Insights
Cyclooxygenase-2 (COX-2) is involved in inflammation and pain but its role in atherosclerosis is uncertain. Selective COX-2 inhibitors may increase cardiovascular risk, highlighting the need for further research.
Area of Science:
- Cardiovascular Science
- Inflammation Biology
- Pharmacology
Background:
- Cyclooxygenase-2 (COX-2) is implicated in inflammation, pain, and physiological functions in tissues like the kidney and endothelium.
- The precise role of COX-2 in atherosclerosis remains unclear, despite existing evidence.
- Clinical trials of selective COX-2 inhibitors have indicated a potential increase in cardiovascular risk.
Purpose of the Study:
- To review the expression patterns of COX-2 in atherothrombosis.
- To elucidate the role of COX-2 in determining plaque vulnerability.
- To examine the vascular effects of prostanoid inhibition by COX-2 inhibitors.
Main Methods:
- Review of existing literature on COX-2 expression in cardiovascular disease.
- Analysis of data from clinical trials concerning selective COX-2 inhibitors.
- Examination of the molecular mechanisms linking COX-2 to atherothrombosis.
Main Results:
- COX-2 is expressed in key cellular components of atherothrombosis.
- COX-2 activity influences atherosclerotic plaque stability and vulnerability.
- Selective COX-2 inhibition affects vascular prostanoid synthesis and may increase cardiovascular risk.
Conclusions:
- The role of COX-2 in atherosclerosis is complex and warrants further investigation.
- The cardiovascular risks associated with selective COX-2 inhibitors necessitate careful consideration.
- Understanding COX-2's vascular effects is crucial for developing safer anti-inflammatory therapies.
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