Abstract
A soluble epoxide hydrolase (sEH) mediates the metabolism of epoxy fatty acids to form the corresponding vicinal diols, which are usually inactive or less active than the epoxide substrates. The sEH enzyme presents in many organs, including but not limited to the liver, heart, spleen, lung, and kidney. Here we summarized the changes in the expression and activity of sEH in multiple renal diseases, such as acute kidney injury (AKI), diabetic nephrology (DN), chronic kidney diseases (CKD), hypertension-mediated renal damage, and other renal dysfunctions. We also discussed the pharmacologic effects and the underlying mechanisms of sEH inhibition by using an inhibitor of sEH and/or the generic deletion of sEH on multiple renal diseases. We believe that sEH is a potential therapeutic target for renal dysfunction although the target disease needs further investigation.
Highlights
A soluble epoxide hydrolase, a member of epoxide hydrolases (EH) family, presents in almost all living organisms (Newman et al, 2005; Morisseau and Hammock, 2013)
SEH is encoded by the gene EPHX2 (Larsson et al, 1995; Sandberg and Meijer, 1996)
The epoxids that could serve as the substrates for a soluble epoxide hydrolase (sEH) have been well documented previously, one member of which is epoxy fatty acids, such as the epoxy metabolites of polyunsaturated fatty acid (PUFA), including but not limited to linoleic acid [LA, 18:2 (n−6)], arachidonic acid [ARA, 20:4 (n−6)], alpha-linolenic acid [ALA,18:3 (n−3)], eicosapentaenoic acid [EPA, 20:5 (n−3)], and docosahexaenoic acid [DHA, 22:6 (n−3)] (Figure 1; Newman et al, 2005)
Summary
A soluble epoxide hydrolase (sEH), a member of epoxide hydrolases (EH) family, presents in almost all living organisms (Newman et al, 2005; Morisseau and Hammock, 2013). The sEH-mediated diol metabolites of epoxide fatty acids are usually inactive or less active than their respective epoxide precursors (Newman et al, 2005; Morisseau and Hammock, 2013). Tissue levels of active epoxy fatty acids could be stabilized by both pharmacological interventions of an inhibitor of sEH and target gene disruption of EPHX2. The expression and activity were reported upregulated in many kidney diseases for human and animals. The enzyme sEH was expressed in all the organs investigated including but not limited to liver, kidney, brain, stomach, intestines, pancreas, prostate, heart, lung, and skin. The sEH has been reported to present in human and animal kidneys at both transcription and protein levels (Table 1).
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