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Nephrol Dial Transplant (2001) 16: 2286-2289
© 2001 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Cyclooxygenase-2 and atherosclerosis: friend or foe?

Ziad A. Massy1 and Suzanne K. Swan1,2,

1 INSERM U507, Necker Hospital and CH Beauvais, Paris, France and 2 Division of Nephrology, Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota, USA

Keywords: atherosclerosis; cyclooxygenase-2

Introduction

Atherosclerosis, manifested by heart disease, stroke, and peripheral vascular disease, remains the leading cause of morbidity and mortality in industrialized countries despite aggressive vascular intervention and myriad blood pressure- and lipid-lowering agents. Over the past decade, however, our understanding of atherogenesis has evolved from one of occlusive lipid accumulation to one of chronic inflammation involving cellular proliferation [1].

Prostaglandins mediate inflammation locally and modulate physiological responses systemically. Nearly all tissues produce prostaglandins and increase production at sites of inflammation. Specifically, arachidonic acid is metabolized to prostaglandin G2 (PGG2) and then to prostaglandin H2 (PGH2) by cyclooxygenase. These moieties are then converted to PGD2, PGE2, PGF2, PGI2, or thromboxane (TBX). The specific prostaglandin produced is determined, in part, by the particular cell type under consideration. For example, endothelium primarily produces PGI2 or prostacyclin, while platelets produce TBX. Despite recognition of cyclooxygenase's mechanism of action 30 years ago [2. . . [Full Text of this Article]

COX-2 and atheromatous tissue

Oxidative stress and COX-2

Prostacyclin (PGI2) and thromboxane (TBX)

Conclusion

Notes

References


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