Evidence map›Paper›PMID 25375931›Full record

ArticlePloS one2014

Oxygen pathway modeling estimates high reactive oxygen species production above the highest permanent human habitation.

Isaac Cano, Vitaly Selivanov, David Gomez-Cabrero, Jesper Tegnér, Josep Roca, Peter D Wagner, Marta Cascante

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mitochondrial function at extreme high altitude.The Journal of physiology · 2016
    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

7 authors at 4 institutions in 3 countries.

Isaac CanoCenter for respiratory diagnoses, Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red en Enfermedades Respiratorias (CIBERES) and Universitat de Barcelona, Barcelona, Catalonia, Spain.
Vitaly SelivanovDepartament de Bioquimica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona and Institute of Biomedicine (IBUB), Barcelona, Catalonia, Spain.
David Gomez-CabreroUnit of Computational Medicine of the Center for Molecular Medicine, Karolinska Institutet and Karoliska University Hospital - Department of Medicine, Stockholm, Sweden.
Jesper TegnérUnit of Computational Medicine of the Center for Molecular Medicine, Karolinska Institutet and Karoliska University Hospital - Department of Medicine, Stockholm, Sweden.
Josep RocaCenter for respiratory diagnoses, Hospital Clinic and Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red en Enfermedades Respiratorias (CIBERES) and Universitat de Barcelona, Barcelona, Catalonia, Spain.
Peter D WagnerDivision of Physiology, Pulmonary and Critical Care Medicine, University of California San Diego, San Diego, California, United States of America.
Marta CascanteDepartament de Bioquimica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona and Institute of Biomedicine (IBUB), Barcelona, Catalonia, Spain.
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESKarolinska Institutet · SEUniversitat de Barcelona · ESUniversity of California System · US

Funding

Tissue Imaging, Biochemistry and MorphologyP01HL091830 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WAGNER, PETER D · 2009 to 2013
$10.1M
NHLBI NIH HHS P01 HL091830
6 · The paper itself

Abstract

The production of reactive oxygen species (ROS) from the inner mitochondrial membrane is one of many fundamental processes governing the balance between health and disease. It is well known that ROS are necessary signaling molecules in gene expression, yet when expressed at high levels, ROS may cause oxidative stress and cell damage. Both hypoxia and hyperoxia may alter ROS production by changing mitochondrial Po2 (PmO2). Because PmO2 depends on the balance between O2 transport and utilization, we formulated an integrative mathematical model of O2 transport and utilization in skeletal muscle to predict conditions to cause abnormally high ROS generation. Simulations using data from healthy subjects during maximal exercise at sea level reveal little mitochondrial ROS production. However, altitude triggers high mitochondrial ROS production in muscle regions with high metabolic capacity but limited O2 delivery. This altitude roughly coincides with the highest location of permanent human habitation. Above 25,000 ft., more than 90% of exercising muscle is predicted to produce abnormally high levels of ROS, corresponding to the "death zone" in mountaineering.

Indexed as

AltitudeComputer SimulationHumansMitochondria, MuscleModels, BiologicalMuscle, SkeletalOxidative StressOxygenOxygen ConsumptionReactive Oxygen SpeciesOxygenReactive Oxygen Species

Identifiers

PMID25375931
PMCPMC4222897
OpenAlexW2108011857

What OpenQuestion holds

Textmetadata
LicenceCC0
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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.