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Arachidonic Acid Metabolism as a Potential Mediator of Cardiac Fibrosis Associated with Inflammation

Scott P. Levick^*, David C. Loch^,, Stephen M. Taylor and Joseph S. Janicki^1,*

^* Cell and Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC 29208; Department of Physiology and Pharmacology, School of Biomedical Sciences, University of Queensland, Brisbane, Australia; and Centre for Systems Biology, Faculty of Sciences, University of Southern Queensland, Toowoomba, Australia

An increase in left ventricular collagen (cardiac fibrosis) is a detrimental process that adversely affects heart function. Strong evidence implicates the infiltration of inflammatory cells as a critical part of the process resulting in cardiac fibrosis. Inflammatory cells are capable of releasing arachidonic acid, which may be further metabolized by cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase enzymes to biologically active products, including PGs, leukotrienes, epoxyeicosatrienoic acids, and hydroxyeicosatetraenoic acids. Some of these products have profibrotic properties and may represent a pathway by which inflammatory cells initiate and mediate the development of cardiac fibrosis. In this study, we critically review the current literature on the potential link between this pathway and cardiac fibrosis.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Address correspondence and reprint requests to Dr. Joseph S. Janicki, Cell and Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC 29208. E-mail address: jjanicki{at}gw.med.sc.edu

² Abbreviations used in this paper: LV, left ventricle; MI, myocardial infarction; AA, arachidonic acid; COX, cyclooxygenase; LO, lipoxygenase; CYP, cytochrome P450 monooxygenase; SHR, spontaneously hypertensive rat; PLA₂, phospholipase A₂; sPLA₂, secretory PLA₂; CysLTs, cysteinyl leukotriene; cPLA_2-, cytosolic PLA_2-; iPLA₂, independent PLA₂; TXA₂, thromboxane A₂; HETE, hydroxyeicosatetraenoic acid; LTB₄, leukotriene B₄; EET, epoxyeicosatrienoic acid.

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