Evidence map›Paper›PMID 28824714›Full record

ArticleTheranostics2017

Cardiac Metabolic Deregulation Induced by the Tyrosine Kinase Receptor Inhibitor Sunitinib is rescued by Endothelin Receptor Antagonism.

Joevin Sourdon, Franck Lager, Thomas Viel, Daniel Balvay, Rebecca Moorhouse, Evangeline Bennana, Gilles Renault, Pierre-Louis Tharaux, Neeraj Dhaun, Bertrand Tavitian

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  2. Review
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  5. Article
  6. Article
  7. The Imaging Value ofMolecular imaging and biology · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Emerging mitochondrial signaling mechanisms in cardio-oncology: beyond oxidative stress.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 2 countries.

Joevin SourdonParis Cardiovascular Research Center (PARCC); INSERM UMR970; Université Paris Descartes; Paris, France.
Franck LagerInstitut Cochin, Université Paris Descartes, INSERM U1016, Paris 75014, France.
Thomas VielParis Cardiovascular Research Center (PARCC); INSERM UMR970; Université Paris Descartes; Paris, France.
Daniel BalvayParis Cardiovascular Research Center (PARCC); INSERM UMR970; Université Paris Descartes; Paris, France.
Rebecca MoorhouseUniversity/British Heart Foundation Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, United Kingdom.
Evangeline BennanaInstitut Cochin, Université Paris Descartes, INSERM U1016, Paris 75014, France.
Gilles RenaultInstitut Cochin, Université Paris Descartes, INSERM U1016, Paris 75014, France.
Pierre-Louis TharauxParis Cardiovascular Research Center (PARCC); INSERM UMR970; Université Paris Descartes; Paris, France.
Neeraj DhaunUniversity/British Heart Foundation Centre of Research Excellence, The Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
Bertrand TavitianParis Cardiovascular Research Center (PARCC); INSERM UMR970; Université Paris Descartes; Paris, France.
Paris Cardiovascular Research Center · FRInstitut Cochin · FRBritish Heart Foundation · GBUniversity of Edinburgh · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The growing field of cardio-oncology addresses the side effects of cancer treatment on the cardiovascular system. Here, we explored the cardiotoxicity of the antiangiogenic therapy, sunitinib, in the mouse heart from a diagnostic and therapeutic perspective. We showed that sunitinib induces an anaerobic switch of cellular metabolism within the myocardium which is associated with the development of myocardial fibrosis and reduced left ventricular ejection fraction as demonstrated by echocardiography. The capacity of positron emission tomography with [

Indexed as

AnaerobiosisAnimalsAntineoplastic AgentsEndothelin Receptor AntagonistsGlycolysisIndolesMice, Inbred C57BLMyocardiumProteomePyrrolesReceptor Protein-Tyrosine KinasesSunitinibAntineoplastic AgentsEndothelin Receptor AntagonistsIndolesProteomePyrrolesReceptor Protein-Tyrosine KinasesSunitinibcardio-oncologycardiotoxicityechocardiographyendothelinmacitentan.positron emission tomographysunitinib

Identifiers

PMID28824714
PMCPMC5562214
OpenAlexW2735591255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.