Document Detail


Targeting epoxides for organ damage in hypertension.
MedLine Citation:
PMID:  20531214     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epoxyeicosatrienoic acids (EETs) are synthesized from arachidonic acid and EETs have a number of beneficial cardiovascular actions. This has led to the concept that EETs and its metabolic pathway can be therapeutically targeted for hypertension and other cardiovascular diseases. One approach has been to prevent the conversion of EETs to their inactive diols by inhibiting the soluble epoxide hydrolase (sEH) enzyme. Inhibition of sEH has been demonstrated to decrease blood pressure in certain experimental models of hypertension, decrease inflammation, and protect organs from damage associated with hypertension and other cardiovascular diseases. The development of sEH inhibitors has reached the point where they are being evaluated in humans. A second therapeutic approach has been to develop EET agonists. EET agonists have been essential for determining the structure function relationship for EETs and determining cell-signaling mechanisms by which EETs exert their cardiovascular actions. More recently, EET agonists have been administered chronically to experimental animal models of hypertension and metabolic syndrome and have been demonstrated to decrease blood pressure, improve insulin signaling, and improve vascular function. These experimental findings provide evidence for sEH inhibitors and EET agonists as a therapeutic approach for cardiovascular diseases, hypertension, and the associated end-organ damage.
Authors:
John D Imig
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  56     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-13     Completed Date:  2011-03-10     Revised Date:  2012-05-07    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  329-35     Citation Subset:  IM    
Affiliation:
Department of Pharmacology & Toxicology, Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA. jdimig@mcw.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Eicosanoids / agonists,  metabolism*
Epoxide Hydrolases / antagonists & inhibitors*,  metabolism
Epoxy Compounds / metabolism*
Humans
Hypertension / drug therapy*,  enzymology,  physiopathology
Molecular Targeted Therapy
Grant Support
ID/Acronym/Agency:
DK38226/DK/NIDDK NIH HHS; HL59699/HL/NHLBI NIH HHS; P01 DK038226-25/DK/NIDDK NIH HHS; R01 HL059699-13/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Eicosanoids; 0/Epoxy Compounds; EC 3.3.2.-/Epoxide Hydrolases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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