Faculty Collaboration Database

Arachidonic acid metabolism as a potential mediator of cardiac fibrosis associated with inflammation. J Immunol 2007 Jan 15;178(2):641-6

Date

01/05/2007

Pubmed ID

17202322

DOI

10.4049/jimmunol.178.2.641

Scopus ID

2-s2.0-33846204382 (requires institutional sign-in at Scopus site)   100 Citations

Abstract

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.

Author List

Levick SP, Loch DC, Taylor SM, Janicki JS

MESH terms used to index this publication - Major topics in bold

Animals
Arachidonic Acid
Eicosanoids
Endomyocardial Fibrosis
Humans
Inflammation
Phospholipases A
Signal Transduction