Evidence map›Paper›PMID 27375480›Full record

ArticleFrontiers in pharmacology2016

Inhibition of Soluble Epoxide Hydrolase Limits Mitochondrial Damage and Preserves Function Following Ischemic Injury.

Maria K Akhnokh, Feng Hua Yang, Victor Samokhvalov, Kristi L Jamieson, Woo Jung Cho, Cory Wagg, Abhijit Takawale, Xiuhua Wang, Gary D Lopaschuk, Bruce D Hammock and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  7. Soluble epoxide hydrolase inhibition alleviates chemotherapy induced neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022
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  12. Mitochondrial Dysfunction Secondary to Endoplasmic Reticulum Stress in Acute Myocardial Ischemic Injury in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2020
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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

12 authors at 3 institutions in 3 countries.

Maria K AkhnokhFaculty of Pharmacy and Pharmaceutical Sciences, 2-020M Katz Group Centre for Pharmacy and Health Research, University of Alberta Edmonton, AB, Canada.
Feng Hua YangGuangdong Laboratory Animal Monitoring Institute Guangdong, China.
Victor SamokhvalovFaculty of Pharmacy and Pharmaceutical Sciences, 2-020M Katz Group Centre for Pharmacy and Health Research, University of Alberta Edmonton, AB, Canada.
Kristi L JamiesonFaculty of Pharmacy and Pharmaceutical Sciences, 2-020M Katz Group Centre for Pharmacy and Health Research, University of Alberta Edmonton, AB, Canada.
Woo Jung ChoImaging Core Facility, Faculty of Medicine and Dentistry, University of Alberta Edmonton, AB, Canada.
Cory WaggMazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Pharmacology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
Abhijit TakawaleMazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Physiology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
Xiuhua WangMazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Physiology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
Gary D LopaschukMazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Pharmacology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada; Department of Pediatrics, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
Bruce D HammockDepartment of Entomology and Nematology Comprehensive Cancer Center, University of California, Davis Davis, CA, USA.
Zamaneh KassiriMazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Physiology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
John M SeubertFaculty of Pharmacy and Pharmaceutical Sciences, 2-020M Katz Group Centre for Pharmacy and Health Research, University of AlbertaEdmonton, AB, Canada; Mazankowski Alberta Heart Institute, University of AlbertaEdmonton, AB, Canada; Department of Pharmacology, Faculty of Medicine and Dentistry, University of AlbertaEdmonton, AB, Canada.
University of Alberta · CAGuangdong Laboratory Animals Monitoring Institute · CNUniversity of California, Davis · US

Funding

HYDROLYTIC ENZYMES IN THE METABOLISM OF TOXINSR01ES002710 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1985 to 2018
$4.0M
NIEHS NIH HHS R01 ES002710
6 · The paper itself

Abstract

aimsMyocardial ischemia can result in marked mitochondrial damage leading to cardiac dysfunction, as such identifying novel mechanisms to limit mitochondrial injury is important. This study investigated the hypothesis that inhibiting soluble epoxide hydrolase (sEH), responsible for converting epoxyeicosatrienoic acids to dihydroxyeicosatrienoic acids protects mitochondrial from injury caused by myocardial infarction.

methodssEH null and WT littermate mice were subjected to surgical occlusion of the left anterior descending (LAD) artery or sham operation. A parallel group of WT mice received an sEH inhibitor, trans-4-[4-(3-adamantan-1-y1-ureido)-cyclohexyloxy]-benzoic acid (tAUCB; 10 mg/L) or vehicle in the drinking water 4 days prior and 7 days post-MI. Cardiac function was assessed by echocardiography prior- and 7-days post-surgery. Heart tissues were dissected into infarct, peri-, and non-infarct regions to assess ultrastructure by electron microscopy. Complexes I, II, IV, citrate synthase, PI3K activities, and mitochondrial respiration were assessed in non-infarct regions. Isolated working hearts were used to measure the rates of glucose and palmitate oxidation.

resultsEchocardiography revealed that tAUCB treatment or sEH deficiency significantly improved systolic and diastolic function post-MI compared to controls. Reduced infarct expansion and less adverse cardiac remodeling were observed in tAUCB-treated and sEH null groups. EM data demonstrated mitochondrial ultrastructure damage occurred in infarct and peri-infarct regions but not in non-infarct regions. Inhibition of sEH resulted in significant improvements in mitochondrial respiration, ATP content, mitochondrial enzymatic activities and restored insulin sensitivity and PI3K activity.

conclusionInhibition or genetic deletion of sEH protects against long-term ischemia by preserving cardiac function and maintaining mitochondrial efficiency.

Indexed as

acute myocardial infarctionarachidonic acidmitochondrial efficiencysoluble epoxide hydrolase

Identifiers

PMID27375480
PMCPMC4896112
OpenAlexW2410942103

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.