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Mediators of Inflammation
Volume 2009 (2009), Article ID 737282, 6 pages
Review Article

Leukotrienes in Atherosclerosis: New Target Insights and Future Therapy Perspectives

1Cardiology Unit, “San Camillo de Lellis” Hospital, Manfredonia, Foggia, Italy
2Cardiology Unit, University of Foggia, Foggia, Italy
3Cardiology Unit, Catholic University, Roma, Italy
4Department of Biomedical Sciences, University of Chieti, Italy

Received 2 April 2009; Revised 15 July 2009; Accepted 28 October 2009

Academic Editor: Muzamil Ahmad

Copyright © 2009 Graziano Riccioni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Atherosclerosis represents an important chronic inflammatory process associated with several pathophysiological reactions in the vascular wall. The arachidonic acid, released by phospholipase A2, is an important substrate for the production of a group of lipid mediators known as leukotrienes, which induce proinflammatory signaling through the activation of specific BLT and CysLT receptors. The interaction of these substances in the vascular wall determines important morphological alterations like the early lipid retention and the accumulation of foam cells, the development of intimal hyperplasia, and advanced atherosclerotic lesions, and it plays an important role in the rupture of atherosclerotic plaque. Many studies regarding myocardial ischemia and reperfusion show that leukotriene signaling may be involved in the development of ischemic injury. For these, reasons both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested for inducing beneficial effects at different stages of the atherosclerosis process and may represent a new therapeutic target in the treatment of atherosclerotic vessel diseases, in particular in acute coronary syndrome.