Evidence map›Paper›PMID 27048652›Full record

ArticleThe Journal of biological chemistry2016

Compartment-specific Control of Reactive Oxygen Species Scavenging by Antioxidant Pathway Enzymes.

Swati Dey, Agnieszka Sidor, Brian O'Rourke

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Systems-level analyses dissociate genetic regulators of reactive oxygen species and energy production.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Bioenergetic myths of energy transduction in eukaryotic cells.Frontiers in molecular biosciences · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

6 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

3 authors at 2 institutions in 1 country.

Swati DeyFrom the Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205.
Agnieszka SidorFrom the Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205.
Brian O'RourkeFrom the Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205 bor@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

ENERGETIC REGULATION OF CARDIAC ION CHANNELSR37HL054598 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2005 to 2014
$3.7M
Redox Modification of the Arrhythmic Substrate in Heart FailureR01HL105216 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN, TRAYANOVA, NATALIA A. · 2011 to 2014
$3.0M
Novel Mitochondrial Ion TransportersR01HL108917 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI O'ROURKE, BRIAN · 2011 to 2015
$2.3M
NHLBI NIH HHS R01 HL105216NHLBI NIH HHS R01 HL108917NHLBI NIH HHS R37 HL054598
6 · The paper itself

Abstract

Oxidative stress arises from an imbalance in the production and scavenging rates of reactive oxygen species (ROS) and is a key factor in the pathophysiology of cardiovascular disease and aging. The presence of parallel pathways and multiple intracellular compartments, each having its own ROS sources and antioxidant enzymes, complicates the determination of the most important regulatory nodes of the redox network. Here we quantified ROS dynamics within specific intracellular compartments in the cytosol and mitochondria and determined which scavenging enzymes exert the most control over antioxidant fluxes in H9c2 cardiac myoblasts. We used novel targeted viral gene transfer vectors expressing redox-sensitive GFP fused to sensor domains to measure H2O2 or oxidized glutathione. Using genetic manipulation in heart-derived H9c2 cells, we explored the contribution of specific antioxidant enzymes to ROS scavenging and glutathione redox potential within each intracellular compartment. Our findings reveal that antioxidant flux is strongly dependent on mitochondrial substrate catabolism, with availability of NADPH as a major rate-controlling step. Moreover, ROS scavenging by mitochondria significantly contributes to cytoplasmic ROS handling. The findings provide fundamental information about the control of ROS scavenging by the redox network and suggest novel interventions for circumventing oxidative stress in cardiac cells.

Indexed as

AnimalsCell LineFree Radical ScavengersHydrogen PeroxideMitochondriaMyoblasts, CardiacOxidation-ReductionOxidative StressRatsFree Radical ScavengersHydrogen Peroxideantioxidantcell metabolismglutathione peroxidasemitochondriaNADPHperoxiredoxinreactive oxygen species (ROS)redox regulationthioredoxinthioredoxin reductase

Identifiers

PMID27048652
PMCPMC4900267
OpenAlexW2316348002

What OpenQuestion holds

Textmetadata
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.