Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 15, Issue 27, Pages 3116-3132Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161209789058020
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Funding
- Swedish Heart and Lung Foundation
- CMM-Soderberg foundation
- SLL/Karolinska Institutet
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The inflammatory environment within the atherosclerotic lesion stimulates the 5-lipoxygenase pathway of arachidonic acid metabolism, leading to the biosynthesis of the potent lipid inflammatory mediators leukotrienes. The present review summarizes the components of this pathway; the enzymes 5-lipoxygenase (5-LO, ALOX5) with its activating protein, FLAP (ALOX5AP), LTA(4) hydrolase and LTC4 synthase, as well as the receptors for leukotriene B-4 (BLT1 and BLT2) and cysteinyl-leukotrienes (CysLT(1) and CysLT(2)), respectively. Genetic variations within the genes encoding these proteins have been associated with cardiovascular risk. Inhibiting the 5-lipoxygenase pathway through either leukotriene synthesis inhibitors or leukotriene receptor antagonists in experimental models of atherosclerosis has however generated contradictory results. Several inhibitors of the 5-lipoxygenase pathway are now evaluated in clinical trials of patients with cardiovascular disease.
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