Evidence map›Paper›PMID 32040259›Full record

ArticleJournal of cellular and molecular medicine2020

Respiratory chain signalling is essential for adaptive remodelling following cardiac ischaemia.

Marten Szibor, Rolf Schreckenberg, Zemfira Gizatullina, Eric Dufour, Marion Wiesnet, Praveen K Dhandapani, Grazyna Debska-Vielhaber, Juliana Heidler, Ilka Wittig, Tuula A Nyman and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Peroxynitrite regulates ER stress-mediated CaJournal of translational medicine · 2025
    Article
  4. Review
  5. Alternative oxidase blunts pseudohypoxia and photoreceptor degeneration due to RPE mitochondrial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Review
  7. Knockout of the Complex III subunit Uqcrh causes bioenergetic impairment and cardiac contractile dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. 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

20 authors at 9 institutions in 5 countries.

Marten SziborFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID 0000-0003-4029-160X
Rolf SchreckenbergDepartment of Physiology, Justus-Liebig University Giessen, Giessen, Germany.
Zemfira GizatullinaDepartment of Neurology, Otto-von-Guericke-University, Magdeburg, Germany.ORCID 0000-0003-2240-4471
Eric DufourFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID 0000-0001-6690-5329
Marion WiesnetDepartment Cardiac Development and Remodelling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Praveen K DhandapaniFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID 0000-0002-3486-4355
Grazyna Debska-VielhaberDepartment of Neurology, Otto-von-Guericke-University, Magdeburg, Germany.ORCID 0000-0002-6661-9821
Juliana HeidlerFunctional Proteomics, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany.ORCID 0000-0003-2607-2849
Ilka WittigFunctional Proteomics, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany.ORCID 0000-0002-9751-8054
Tuula A NymanDepartment of Immunology, Institute of Clinical Medicine, Oslo University Hospital, University of Oslo, Oslo, Norway.ORCID 0000-0001-8787-5886
Ulrich GärtnerInstitute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, Giessen, Germany.
Andrew R HallMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.
Victoria PellDepartment of Medicine, University of Cambridge, Cambridge, UK.
Carlo ViscomiMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0001-6050-0566
Thomas KriegDepartment of Medicine, University of Cambridge, Cambridge, UK.ORCID 0000-0002-5192-580X
Michael P MurphyMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.
Thomas BraunDepartment Cardiac Development and Remodelling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Frank N GellerichDepartment of Neurology, Otto-von-Guericke-University, Magdeburg, Germany.ORCID 0000-0002-6550-4555
Klaus-Dieter SchlüterDepartment of Physiology, Justus-Liebig University Giessen, Giessen, Germany.ORCID 0000-0002-6093-4919
Howard T JacobsFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID 0000-0003-1895-6003
University of Cambridge · GBJustus-Liebig-Universität Gießen · DEOtto-von-Guericke-Universität Magdeburg · DEUniversity of Helsinki · FIGoethe University Frankfurt · DEMax Planck Institute for Heart and Lung Research · DEOslo University Hospital · NOTampere University · FIUniversity of Padua · IT

Funding

European Research Council 232738Medical Research Council MC_EX_MR/P007031/1Medical Research Council MC_U105663142Medical Research Council MC_UP_1002/1Medical Research Council MC_UU_00015/3Medical Research Council MC_UU_00015/5Medical Research Council MC_UU_00015/7Medical Research Council MC_UU_00015/8MRF_ MRF-155-0002-RG-ZEVIAMRF_ MRF-175-0001-RG-ZEVI-C0898Wellcome Trust 110158/Z/15/ZWellcome Trust 110159/Z/15/Z
6 · The paper itself

Abstract

Cardiac ischaemia-reperfusion (I/R) injury has been attributed to stress signals arising from an impaired mitochondrial electron transport chain (ETC), which include redox imbalance, metabolic stalling and excessive production of reactive oxygen species (ROS). The alternative oxidase (AOX) is a respiratory enzyme, absent in mammals, that accepts electrons from a reduced quinone pool to reduce oxygen to water, thereby restoring electron flux when impaired and, in the process, blunting ROS production. Hence, AOX represents a natural rescue mechanism from respiratory stress. This study aimed to determine how respiratory restoration through xenotopically expressed AOX affects the re-perfused post-ischaemic mouse heart. As expected, AOX supports ETC function and attenuates the ROS load in post-anoxic heart mitochondria. However, post-ischaemic cardiac remodelling over 3 and 9 weeks was not improved. AOX blunted transcript levels of factors known to be up-regulated upon I/R such as the atrial natriuretic peptide (Anp) whilst expression of pro-fibrotic and pro-apoptotic transcripts were increased. Ex vivo analysis revealed contractile failure at nine but not 3 weeks after ischaemia whilst label-free quantitative proteomics identified an increase in proteins promoting adverse extracellular matrix remodelling. Together, this indicates an essential role for ETC-derived signals during cardiac adaptive remodelling and identified ROS as a possible effector.

Indexed as

Signal TransductionVentricular RemodelingAlternative OxidaseAnimalsBiocatalysisElectron TransportExtracellular MatrixMaleMiceMitochondria, HeartMitochondrial ProteinsMyocardial ContractionMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumOxidoreductasesAlternative OxidaseMitochondrial ProteinsOxidoreductasesPlant ProteinsRNA, Messengeradaptive cardiac remodellingalternative oxidasecardiac ischaemia-reperfusionelectron transport chainmousereactive oxygen species

Identifiers

PMID32040259
PMCPMC7131948
OpenAlexW3004889911

What OpenQuestion holds

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LicenceCC BY
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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.