
Epoxyeicosatrienoic acids (EETs) are arachidonic acid metabolites that importantly contribute to vascular and cardiac physiology. The contribution of EETs to vascular and cardiac function is further influenced by soluble epoxide hydrolase (sEH) that degrades EETs to diols. Vascular actions of EETs include dilation and angiogenesis. EETs also decrease inflammation and platelet aggregation and in general act to maintain vascular homeostasis. Myocyte contraction and increased coronary blood flow are the two primary EET actions in the heart. EET cell signaling mechanisms are tissue and organ specific and provide significant evidence for the existence of EET receptors. Additionally, pharmacological and genetic manipulations of EETs and sEH have demonstrated a contribution for this metabolic pathway to cardiovascular diseases. Given the impact of EETs to cardiovascular physiology, there is emerging evidence that development of EET-based therapeutics will be beneficial for cardiovascular diseases.
Epoxide Hydrolases, Platelet Aggregation, Neovascularization, Physiologic, Cardiovascular Physiological Phenomena, Vasodilation, Animals, Epoxy Compounds, Homeostasis, Humans, Signal Transduction
Epoxide Hydrolases, Platelet Aggregation, Neovascularization, Physiologic, Cardiovascular Physiological Phenomena, Vasodilation, Animals, Epoxy Compounds, Homeostasis, Humans, Signal Transduction
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