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Soluble epoxide hydrolase: gene structure, expression and deletion.

Todd R Harris1, Bruce D Hammock

  • 1Department of Entomology and Comprehensive Cancer Center, University of California, Davis, CA 95616, USA.

Gene
|May 25, 2013
PubMed
Summary

Soluble epoxide hydrolase (sEH) metabolizes lipid signaling molecules like epoxyeicosatrienoic acids (EETs), impacting vascular tone and inflammation. Targeting sEH offers a therapeutic strategy for diseases including hypertension and pain.

Keywords:
20-HETE20-hydroxyeicosatetraenoic acid5-lipoxygenase activation proteinAP-1ARICATF-6Ang-IIAtherosclerosis Risk in CommunitiesCACCARDIACPRChIPCoronary Artery Risk Development in Young AdultsDHADHETsEETsEPAEPHX2EpFAsEpoxyeicosatrienoic acidFLAPGSISHUVECsHcyHypertensionIBDIL-10InflammationLPSLipid signalingNSAIDOVXPPARsRAASRBCSHRSNPsSP-1STZTHFUPREsUTRVSMWKYWistar-Kyotoactivating transcription factor-6activator protein 1angiotensin IIcardiopulmonary resuscitationchromatin immunoprecipitationcoronary artery calcificationdihydroxyeicosatrienoic acidsdocosahexaenoic acideNOSeicosapentaenoic acidendothelial nitric oxide synthaseepoxy-fatty acidsepoxyeicosatrienoic acidsglucose-stimulated insulin secretionhomocysteinehuman umbilical vein endothelial cellsinflammatory bowel diseaseinterleukin-10lipopolysaccharidenonsteroidal anti-inflammatory drugovariectomizedperoxisome-proliferator activated receptorsred blood cellrenin–angiotensin aldosterone systemsEHsingle nucleotide polymorphismssoluble epoxide hydrolasespecificity protein 1spontaneously hypertensive ratstreptozotocintetrahydrofuranunfolded protein response elementsuntranslated regionvascular smooth muscle

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Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Mammalian soluble epoxide hydrolase (sEH) is a key enzyme in lipid metabolism.
  • sEH hydrolyzes epoxyeicosatrienoic acids (EETs), which are derived from arachidonic acid.
  • EETs play crucial roles in regulating vascular tone, nociception, angiogenesis, and inflammation.

Purpose of the Study:

  • To review the structure, function, evolution, and gene structure of sEH.
  • To discuss the role of sEH in various disease models, including human genetic variations and gene expression.
  • To summarize findings from studies utilizing the sEH knockout mouse model.

Main Methods:

  • Literature review of sEH protein structure and function.
  • Analysis of sEH evolution and gene structure.
  • Examination of human single nucleotide polymorphisms and mammalian gene expression in disease contexts.
  • Overview of sEH knockout mouse model studies.

Main Results:

  • sEH is central to the metabolism of lipid mediators, influencing key physiological processes.
  • Dysregulation of sEH is implicated in pathological conditions such as cardiac hypertrophy, diabetes, hypertension, and pain.
  • The sEH knockout mouse model has been instrumental in understanding its physiological and pathological roles.

Conclusions:

  • sEH is a significant therapeutic target due to its involvement in multiple disease states.
  • Understanding sEH's multifaceted roles provides insights into potential treatment strategies for cardiovascular and inflammatory diseases.
  • Further research, including studies with knockout models, is crucial for developing sEH-targeted therapies.