Evidence map›Paper›PMID 28598967›Full record

ArticlePLoS computational biology2017

Mitochondrial respiration and ROS emission during β-oxidation in the heart: An experimental-computational study.

Sonia Cortassa, Steven J Sollott, Miguel A Aon

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.9field-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

40 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. The role of CD36 in cardiovascular disease.Cardiovascular research · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Sonia CortassaLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States of America.ORCID http://orcid.org/0000-0001-7224-9858
Steven J SollottLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States of America.
Miguel A AonLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States of America.ORCID http://orcid.org/0000-0002-4355-5431
National Institutes of Health · US

Funding

Control Mechanisms for Matching ATP Supply and Demand in Heart MitochondriaZIAAG000250 · NIA · NATIONAL INSTITUTE ON AGING · PI SOLLOTT, STEVEN · 2009 to 2024
$21.0M
6 · The paper itself

Abstract

Lipids are main fuels for cellular energy and mitochondria their major oxidation site. Yet unknown is to what extent the fuel role of lipids is influenced by their uncoupling effects, and how this affects mitochondrial energetics, redox balance and the emission of reactive oxygen species (ROS). Employing a combined experimental-computational approach, we comparatively analyze β-oxidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from Sham and streptozotocin (STZ)-induced type 1 diabetic (T1DM) guinea pigs (GPs). Parallel high throughput measurements of the rates of oxygen consumption (VO2) and hydrogen peroxide (H2O2) emission as a function of PCoA concentration, in the presence of L-carnitine and malate, were performed. We found that PCoA concentration < 200 nmol/mg mito protein resulted in low H2O2 emission flux, increasing thereafter in Sham and T1DM GPs under both states 4 and 3 respiration with diabetic mitochondria releasing higher amounts of ROS. Respiratory uncoupling and ROS excess occurred at PCoA > 600 nmol/mg mito prot, in both control and diabetic animals. Also, for the first time, we show that an integrated two compartment mitochondrial model of β-oxidation of long-chain fatty acids and main energy-redox processes is able to simulate the relationship between VO2 and H2O2 emission as a function of lipid concentration. Model and experimental results indicate that PCoA oxidation and its concentration-dependent uncoupling effect, together with a partial lipid-dependent decrease in the rate of superoxide generation, modulate H2O2 emission as a function of VO2. Results indicate that keeping low levels of intracellular lipid is crucial for mitochondria and cells to maintain ROS within physiological levels compatible with signaling and reliable energy supply.

Indexed as

Lipid MetabolismModels, CardiovascularAnimalsCell RespirationCells, CulturedComputer SimulationDiabetes MellitusElectron TransportGuinea PigsHydrogen PeroxideMaleMetabolismMitochondria, HeartOxidation-ReductionOxygenPalmitoyl Coenzyme AHydrogen PeroxideOxygenPalmitoyl Coenzyme AReactive Oxygen Species

Identifiers

PMID28598967
PMCPMC5482492
OpenAlexW2622164463

What OpenQuestion holds

Textmetadata
LicenceCC0
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.