Abstract
Arachidonic acid (AA) is an essential fatty acid that is released by phospholipids in cell membranes and metabolized by cyclooxygenase (COX), cytochrome P450 (CYP) enzymes, and lipid oxygenase (LOX) pathways to regulate complex cardiovascular function under physiological and pathological conditions. Various AA metabolites include prostaglandins, prostacyclin, thromboxanes, hydroxyeicosatetraenoic acids, leukotrienes, lipoxins, and epoxyeicosatrienoic acids. The AA metabolites play important and differential roles in the modulation of vascular tone, and cardiovascular complications including atherosclerosis, hypertension, and myocardial infarction upon actions to different receptors and vascular beds. This article reviews the roles of AA metabolism in cardiovascular health and disease as well as their potential therapeutic implication.
Highlights
It is noteworthy that arachidonic acid (AA), one of the most abundant Polyunsaturated fatty acids (PUFAs) in the human body, is a longchain polyunsaturated omega-6 fatty acid containing 20 carbon atoms and 4 double bonds
These results indicate that AA is abundant in various food items
These findings imply a close linkage between AA metabolites, COX-2 activity, and vascular complications associated with diabetes and obesity
Summary
Upon binding to corresponding receptors and triggering the downstream signaling pathways in different tissues, AA metabolites play differential roles to control important cellular processes, such as cell apoptosis, cell proliferation, metabolism, and vascular function [7,13], and they are related to many chronic diseases, especially cardiovascular diseases (CVD) [14,15]. Studies have shown that AA metabolites play an important role in cardiovascular health and disease mechanism, especially related to inflammation and atherosclerosis [15]. AA metabolites regulate the complex vascular functions in the human body and play a role in the treatment of CVD. The current article reviews the comprehensive involvement of AA metabolites in cardiovascular function, from the differential signaling pathways mediated to their potential therapeutic implications
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