Evidence map›Paper›PMID 23701967›Full record

ReviewGene2013

Soluble epoxide hydrolase: gene structure, expression and deletion.

Todd R Harris, Bruce D Hammock

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

133 citing papers in PubMed, 1 synthesis or guideline pooled it, 228 citations in OpenAlex.

  1. Pooled it
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  12. Impacts of Oxylipins on ischemic stroke: from pathophysiology to clinical phenotypes.Metabolomics : Official journal of the Metabolomic Society · 2025
    Review
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73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Todd R HarrisDepartment of Entomology and Comprehensive Cancer Center, University of California, Davis, CA 95616, USA.
Bruce D Hammock
University of California, Davis · US

Funding

Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR37ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1998 to 2007
$3.0M
NHLBI NIH HHS T32 HL086350NHLBI NIH HHS T32 HL86350NIEHS NIH HHS R01 ES002710NIEHS NIH HHS R37 ES002710NIEHS NIH HHS R37 ES02710
6 · The paper itself

Abstract

Mammalian soluble epoxide hydrolase (sEH) converts epoxides to their corresponding diols through the addition of a water molecule. sEH readily hydrolyzes lipid signaling molecules, including the epoxyeicosatrienoic acids (EETs), epoxidized lipids produced from arachidonic acid by the action of cytochrome p450s. Through its metabolism of the EETs and other lipid mediators, sEH contributes to the regulation of vascular tone, nociception, angiogenesis and the inflammatory response. Because of its central physiological role in disease states such as cardiac hypertrophy, diabetes, hypertension, and pain sEH is being investigated as a therapeutic target. This review begins with a brief introduction to sEH protein structure and function. sEH evolution and gene structure are then discussed before human small nucleotide polymorphisms and mammalian gene expression are described in the context of several disease models. The review ends with an overview of studies that have employed the sEH knockout mouse model.

Indexed as

AnimalsCatalysisDisease Models, AnimalEpoxide HydrolasesEvolution, MolecularGene ExpressionGene Expression RegulationHumansMiceMice, KnockoutPolymorphism, Single NucleotideProtein ConformationSequence DeletionEpoxide Hydrolases20-HETE20-hydroxyeicosatetraenoic acid5-lipoxygenase activation proteinactivating transcription factor-6activator protein 1Ang-IIangiotensin IIAP-1ARICATF-6Atherosclerosis Risk in CommunitiesCACCARDIAcardiopulmonary resuscitationChIPchromatin immunoprecipitationcoronary artery calcificationCoronary Artery Risk Development in Young AdultsCPRDHADHETsdihydroxyeicosatrienoic acidsdocosahexaenoic acidEETseicosapentaenoic acidendothelial nitric oxide synthaseeNOSEPAEpFAsEPHX2Epoxyeicosatrienoic acidepoxyeicosatrienoic acidsepoxy-fatty acidsFLAPglucose-stimulated insulin secretionGSISHcyhomocysteinehuman umbilical vein endothelial cellsHUVECsHypertensionIBDIL-10Inflammationinflammatory bowel diseaseinterleukin-10Lipid signalinglipopolysaccharideLPSnonsteroidal anti-inflammatory drugNSAIDovariectomizedOVXperoxisome-proliferator activated receptorsPPARsRAASRBCred blood cellrenin–angiotensin aldosterone systemsEHSHRsingle nucleotide polymorphismsSNPssoluble epoxide hydrolaseSP-1specificity protein 1spontaneously hypertensive ratstreptozotocinSTZtetrahydrofuranTHFunfolded protein response elementsuntranslated regionUPREsUTRvascular smooth muscleVSMWistar-KyotoWKY

Identifiers

PMID23701967
PMCPMC3733540
OpenAlexW2030824198

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.