Evidence map›Paper›PMID 27494529›Full record

ArticlePloS one2016

Novel Roles of Epoxyeicosanoids in Regulating Cardiac Mitochondria.

Haitham E El-Sikhry, Nasser Alsaleh, Rambabu Dakarapu, John R Falck, John M Seubert

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Mechanism of CREB1 in cardiac function of rats with heart failure via regulating the microRNA-376a-3p/TRAF6 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
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  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Orally Active Epoxyeicosatrienoic Acid Analogs.Journal of cardiovascular pharmacology · 2017
    Review
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

5 authors.

Haitham E El-SikhryFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada.
Nasser AlsalehFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada.
Rambabu DakarapuDepartments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
John R FalckDepartments of Biochemistry and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America.
John M SeubertFaculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, AB, Canada.

Funding

TRANSPORT EFFECTS OF ARACHIDONATE METABOLITES IN PERFUSED TUBULEP01DK038226 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BROWN, NANCY J. · 1986 to 2015
$22.1M
NIDDK NIH HHS P01 DK038226
6 · The paper itself

Abstract

Maintenance of a healthy pool of mitochondria is important for the function and survival of terminally differentiated cells such as cardiomyocytes. Epoxyeicosatrienoic acids (EETs) are epoxy lipids derived from metabolism of arachidonic acid by cytochrome P450 epoxygenases. We have previously shown that EETs trigger a protective response limiting mitochondrial dysfunction and reducing cellular death. The aim of this study was to investigate whether EET-mediated effects influence mitochondrial quality in HL-1 cardiac cells during starvation. HL-1 cells were subjected to serum- and amino acid free conditions for 24h. We employed a dual-acting synthetic analog UA-8 (13-(3-propylureido)tridec-8-enoic acid), possessing both EET-mimetic and soluble epoxide hydrolase (sEH) inhibitory properties, or 14,15-EET as model EET molecules. We demonstrated that EET-mediated events significantly improved mitochondrial function as assessed by preservation of the ADP/ATP ratio and oxidative respiratory capacity. Starvation induced mitochondrial hyperfusion observed in control cells was attenuated by UA-8. However, EET-mediated events did not affect the expression of mitochondrial dynamic proteins Fis1, DRP-1 or Mfn2. Rather we observed increased levels of OPA-1 oligomers and increased mitochondrial cristae density, which correlated with the preserved mitochondrial function. Increased DNA binding activity of pCREB and Nrf1/2 and increased SIRT1 activity together with elevated mitochondrial proteins suggest EET-mediated events led to preserved mitobiogenesis. Thus, we provide new evidence for EET-mediated events that preserve a healthier pool of mitochondria in cardiac cells following starvation-induced stress.

Indexed as

8,11,14-Eicosatrienoic AcidAconitate HydrataseCell LineCyclic AMP Response Element-Binding ProteinGTP PhosphohydrolasesHumansMitochondria, HeartNF-E2-Related Factor 2Nuclear Respiratory Factor 1Oleic AcidsSirtuin 1(13-(3-propylureido)tridec-8-enoic acid)14,15-eicosa-5-enoic acid14,15-epoxy-5,8,11-eicosatrienoic acid8,11,14-Eicosatrienoic AcidAconitate HydrataseCREB1 protein, humanCyclic AMP Response Element-Binding ProteinGTP PhosphohydrolasesNFE2L2 protein, humanNF-E2-Related Factor 2NRF1 protein, humanNuclear Respiratory Factor 1Oleic AcidsOPA1 protein, humanSIRT1 protein, humanSirtuin 1

Identifiers

PMID27494529
PMCPMC4975494

What OpenQuestion holds

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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.