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. 2016 Dec 20;4(12):e1151. doi: 10.1097/GOX.0000000000001151

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Copyright © 2016 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The American Society of Plastic Surgeons. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Fig. 1. — Epoxyeicosatrienoic acid formation and metabolism by soluble epoxide hydrolase. Upon activation of cells by external stimuli, arachidonic acid is released from membrane phospholipids by phospholipase A2 (PLA2). Arachidonic acid is also derived from dietary linoleic acid. Arachidonic acid can be metabolized along one of 3 pathways: the cyclooxygenase (COX) pathway, the lipoxygenase (LOX) pathway, or the CYP pathway. CYP epoxygenases metabolize arachidonic acid to produce EETs. These have been shown to act as autocrine and paracrine mediators with proangiogenic, antihypertensive, and antiinflammatory activities. These properties of EETs are attenuated by their metabolism to DiHETEs by the enzyme sEH. sEHIs prevent the metabolism of EETs to DiHETEs leading to EET accumulation.