Evidence map›Paper›PMID 26722838›Full record

ArticleRedox biology2016

Fatty acid nitroalkenes induce resistance to ischemic cardiac injury by modulating mitochondrial respiration at complex II.

Jeffrey R Koenitzer, Gustavo Bonacci, Steven R Woodcock, Chen-Shan Chen, Nadiezhda Cantu-Medellin, Eric E Kelley, Francisco J Schopfer

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Nitro Fatty Acids (NOMolecules (Basel, Switzerland) · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
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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

7 authors at 1 institution in 1 country.

Jeffrey R KoenitzerDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Gustavo BonacciDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Steven R WoodcockDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Chen-Shan ChenDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Nadiezhda Cantu-MedellinDepartment of Anesthesiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Eric E KelleyDepartment of Anesthesiology, University of Pittsburgh, Pittsburgh, PA 15261, USA.
Francisco J SchopferDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA 15261, USA. Electronic address: fjs2@pitt.edu.
University of Pittsburgh · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Formation of Omega 3-Derived Electrophiles During InflammationR01AT006822 · NCCIH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SCHOPFER, FRANCISCO JOSE · 2011 to 2015
$1.8M
NCCIH NIH HHS R01 AT006822NCI NIH HHS P30 CA047904
6 · The paper itself

Abstract

Nitro-fatty acids (NO2-FA) are metabolic and inflammatory-derived electrophiles that mediate pleiotropic signaling actions. It was hypothesized that NO2-FA would impact mitochondrial redox reactions to induce tissue-protective metabolic shifts in cells. Nitro-oleic acid (OA-NO2) reversibly inhibited complex II-linked respiration in isolated rat heart mitochondria in a pH-dependent manner and suppressed superoxide formation. Nitroalkylation of Fp subunit was determined by BME capture and the site of modification by OA-NO2 defined by mass spectrometric analysis. These effects translated into reduced basal and maximal respiration and favored glycolytic metabolism in H9C2 cardiomyoblasts as assessed by extracellular H(+) and O2 flux analysis. The perfusion of NO2-FA induced acute cardioprotection in an isolated perfused heart ischemia/reperfusion (IR) model as evidenced by significantly higher rate-pressure products. Together these findings indicate that NO2-FA can promote cardioprotection by inducing a shift from respiration to glycolysis and suppressing reactive species formation in the post-ischemic interval.

Indexed as

Cell RespirationAlkenesAnimalsCardiotonic AgentsCell LineElectron Transport Complex IIElectron Transport Complex IIIFatty AcidsHydrogen-Ion ConcentrationMaleMitochondria, HeartMyoblasts, CardiacMyocardial IschemiaMyocardial Reperfusion InjuryNitric OxideNitro CompoundsAlkenesCardiotonic AgentsElectron Transport Complex IIElectron Transport Complex IIIFatty AcidsNitric OxideNitro CompoundsSuperoxidesElectrophileInflammationMitochondriaNitroalkeneNitro-fatty acid

Identifiers

PMID26722838
PMCPMC4710799
OpenAlexW2220418356

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.