Abstract
Epoxyeicosatrienoic acids (EETs) are metabolites of arachidonic acid by cytochrome P450 (CYP) epoxygenases, which include four regioisomers: 5,6-EET, 8,9-EET, 11,12-EET, and 14,15-EET. Each of them possesses beneficial effects against inflammation, fibrosis, and apoptosis, which could combat cardiovascular diseases. Numerous studies have demonstrated that elevation of EETs by overexpression of CYP2J2, inhibition of sEH, or treatment with EET analogs showed protective effects in various cardiovascular diseases, including hypertension, myocardial infarction, and heart failure. As is known to all, cardiac remodeling is the major pathogenesis of cardiovascular diseases. This review will begin with the introduction of EETs and their protective effects in cardiovascular diseases. In the following, the roles of EETs in cardiac remodeling, with a particular emphasis on myocardial hypertrophy, apoptosis, fibrosis, inflammation, and angiogenesis, will be summarized. Finally, it is suggested that upregulation of EETs is a potential therapeutic strategy for cardiovascular diseases. The EET-related drug development against cardiac remodeling is also discussed, including the overexpression of CYP2J2, inhibition of sEH, and the analogs of EET.
Highlights
Cardiovascular disease (CVD) is recognized as a leading cause of mortality worldwide (Roth et al, 2015)
Oni-Orisan et al (2016) reported that lower epoxyeicosatrienoic acids (EETs) levels including 8,9-EET, 11,12-EET, and 14,15-EET were observed in obstructed coronary artery disease (CAD) patients compared with patients with no apparent CAD, which was consistent with the results reported by Theken et al (2012)
Our laboratory showed that overexpression of CYP2J2 and 11,12-EET attenuated cardiac hypertrophy elicited with Ang angiotensin II (II), which was mediated through the activation of adenosine 5’-monophosphate-activated protein kinase (AMPK)-α2 (Wang et al, 2016)
Summary
Division of Cardiology, Tongji Hospital, Tongji Medical College and Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiologic Disorders, Huazhong University of Science and Technology, Wuhan, China. Numerous studies have demonstrated that elevation of EETs by overexpression of CYP2J2, inhibition of sEH, or treatment with EET analogs showed protective effects in various cardiovascular diseases, including hypertension, myocardial infarction, and heart failure. The roles of EETs in cardiac remodeling, with a particular emphasis on myocardial hypertrophy, apoptosis, fibrosis, inflammation, and angiogenesis, will be summarized. The EET-related drug development against cardiac remodeling is discussed, including the overexpression of CYP2J2, inhibition of sEH, and the analogs of EET.
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