Arachidonic acid metabolism as a potential mediator of cardiac fibrosis associated with inflammation.
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.
Levick
Scott P
SP
Cell and Developmental Biology and Anatomy, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.
Loch
David C
DC
Taylor
Stephen M
SM
Janicki
Joseph S
JS
D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism*; D015777:Eicosanoids / Q000378:metabolism; D004719:Endomyocardial Fibrosis / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D010741:Phospholipases A / Q000378:metabolism; D015398:Signal Transduction
D015777:Eicosanoids; D016718:Arachidonic Acid; D010741:Phospholipases A