Evidence map›Paper›PMID 32045716›Full record

ArticleMitochondrion2020

Prophylaxis of mitochondrial dysfunction caused by cellular decompression from hyperbaric exposure.

Abhay Ranganathan, Shawn Owiredu, David H Jang, David M Eckmann

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Landing a Successful R or K Grant: a Young Investigator's Journey.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2021
    Article
  4. 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

4 authors at 1 institution in 1 country.

Abhay RanganathanDepartment of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States.
Shawn OwireduDepartment of Emergency Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States.
David H JangDepartment of Emergency Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States.
David M EckmannDepartment of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States; Department of Bioengineering, School of Engineering and Applied Sciences, University of Pennsylvania, Philadelphia, PA 19104, United States. Electronic address: david.eckmann@osumc.edu.
University of Pennsylvania · US

Funding

Abnormal Mitochondrial Bioenergetic and Motility Signatures in Human Blood Cells as Indices of Acute Poisoning in PatientsK08HL136858 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI JANG, DAVID H · 2018 to 2021
$675k
NHLBI NIH HHS K08 HL136858
6 · The paper itself

Abstract

Mitochondrial dysfunction occurring in response to cellular perturbations can include altered mitochondrial motility and bioenergetic function having intracellular heterogeneity. Exogenous mitochondrial directed therapy may correct these dysfunctions. Using in vitro approaches, we find that cell perturbations induced by rapid decompression from hyperbaric conditions with specific gas exposures has differential effects on mitochondrial motility, inner membrane potential, cellular respiration, reactive oxygen species production, impaired maintenance of cell shape and altered intracellular distribution of bioenergetic capacity in perinuclear and cell peripheral domains. Addition of a first-generation cell-permeable succinate prodrug to support mitochondrial function has positive overall effects in blunting the resultant bioenergy responses. Our results with this model of perturbed cell function induced by rapid decompression indicate that alterations in bioenergetic state are partitioned within the cell, as directly assessed by a combination of mitochondrial respiration and dynamics measurements. Reductions in the observed level of dysfunction produced can be achieved with application of the cell-permeable succinate prodrug.

Indexed as

Cell RespirationCells, CulturedDecompressionEnergy MetabolismHumansHyperbaric OxygenationMembrane Potential, MitochondrialMitochondrial DynamicsMitochondria, MuscleMyocytes, Smooth MuscleNitrogenOxygenPrimary Cell CultureProdrugsReactive Oxygen SpeciesSuccinic AcidNitrogenOxygenProdrugsReactive Oxygen SpeciesSuccinic AcidBioenergeticsDecompressionIntermembrane potentialMicroscopyMitochondriaMotilityPerinuclearRespiration

Identifiers

PMID32045716
PMCPMC7416481
OpenAlexW3005064545

What OpenQuestion holds

Textmetadata
LicenceTDM
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.