In addition to their role as xenobiotic metabolizing enzymes, cytochrome P450 
(CYP) epoxygenases actively contribute to the metabolism of endogenous 
substances such as arachidonic acid. Epoxyeicosatrienoic acids (EETs) are 
epoxide derivative of arachidonic acid. CYP2C8/9 and CYP2J2 are the main 
epoxygenases expressed in human tissues including endothelial cells which are 
the chief sources of EET formation in human body. Once formed, EETs are 
primarily metabolized to their less biologically active metabolites, 
dihydroxyeicosatrienoic acids, by soluble epoxy hydrolase (sEH) enzyme. EETs 
possess a wide range of established protective effects on human cardiovascular 
system of which vasodilatory, angiogenic and anti-inflammatory actions have been 
more extensively described. On the other hand, inflammation has shown to 
decrease the expression and activity of CYP enzyme, including epoxygenases. 
Given the fact that CYP epoxygenase-derive EETs exhibit potent cardiovascular 
protective effects, including anti-inflammation, and that inflammation suppress 
CYP activation and EET formation, it would make sense to speculate that under 
inflammatory conditions there exists an 
inflammation-epoxygenase-EET-inflammation vicious cycle in which the 
inflammation-induced downregulation of CYP epoxygenases causes a decrease in the 
EET production. Insufficient EET synthesis would, in turn, lead to an 
ineffective EET-mediated anti-inflammatory effect, leading to an augmentation of 
systemic and regional inflammatory responses and further downregulation of CYP 
epoxygenase activity/EET production. This cycle, if any, might help to better 
understanding of pathophysiology of chronic cardiovascular diseases and also 
could be an emerging target for further pharmacological therapy of disorders in 
which increased inflammatory responses are known to occur.