Evidence map›Paper›PMID 33350094›Full record

ArticleESC heart failure2021

Muscular changes in animal models of heart failure with preserved ejection fraction: what comes closest to the patient?

Keita Goto, Antje Schauer, Antje Augstein, Mei Methawasin, Henk Granzier, Martin Halle, Emeline M Van Craenenbroeck, Natale Rolim, Stephan Gielen, Burkert Pieske and 3 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023
    Review
  9. Empagliflozin Preserves Skeletal Muscle Function in a HFpEF Rat Model.International journal of molecular sciences · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
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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

13 authors at 8 institutions in 4 countries.

Keita GotoLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Antje SchauerLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Antje AugsteinLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Mei MethawasinDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, USA.
Henk GranzierDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, USA.
Martin HallePrevention and Sports Medicine, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Emeline M Van CraenenbroeckResearch group Cardiovascular Diseases, GENCOR Department, Antwerp University Hospital, Edegem, Belgium.
Natale RolimDepartment of Circulation and Medical Imaging, Faculty of Medicine, NTNU, K.G. Jebsen Center of Exercise in Medicine, Trondheim, Norway.
Stephan GielenDepartment of Cardiology, Angiology and Intensive Care, Klinikum Lippe, Detmold, Germany.
Burkert PieskeDepartment of Internal Medicine and Cardiology Campus Virchow-Klinikum, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Ephraim B WinzerLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Axel LinkeLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Volker AdamsLaboratory for Experimental and Molecular Cardiology, Department of Internal Medicine and Cardiology, TU Dresden, Heart Center Dresden University Hospital, Fetscherstrasse 76, Dresden, 01307, Germany.
Technische Universität Dresden · DEUniversity Hospital Carl Gustav Carus · DEUniversity of Arizona · USAntwerp University Hospital · BECharité - Universitätsmedizin Berlin · DEGerman Centre for Cardiovascular Research · DEKlinikum Lippe · DENorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHeart failure with preserved ejection fraction (HFpEF) is associated with reduced exercise capacity elicited by skeletal muscle (SM) alterations. Up to now, no clear medical treatment advice for HFpEF is available. Identification of the ideal animal model mimicking the human condition is a critical step in developing and testing treatment strategies. Several HFpEF animals have been described, but the most suitable in terms of comparability with SM alterations in HFpEF patients is unclear. The aim of the present study was to investigate molecular changes in SM of three different animal models and to compare them with alterations of muscle biopsies obtained from human HFpEF patients. METHODS AND

resultsSkeletal muscle tissue was obtained from HFpEF and control patients and from three different animal models including the respective controls-ZSF1 rat, Dahl salt-sensitive rat, and transverse aortic constriction surgery/deoxycorticosterone mouse. The development of HFpEF was verified by echocardiography. Protein expression and enzyme activity of selected markers were assessed in SM tissue homogenates. Protein expression between SM tissue obtained from HFpEF patients and the ZSF1 rats revealed similarities for protein markers involved in muscle atrophy (MuRF1 expression, protein ubiquitinylation, and LC3) and mitochondrial metabolism (succinate dehydrogenase and malate dehydrogenase activity, porin expression). The other two animal models exhibited far less similarities to the human samples.

conclusionsNone of the three tested animal models mimics the condition in HFpEF patients completely, but among the animal models tested, the ZSF1 rat (ZSF1-lean vs. ZSF1-obese) shows the highest overlap to the human condition. Therefore, when studying therapeutic interventions to treat HFpEF and especially alterations in the SM, we suggest that the ZSF1 rat is a suitable model.

Indexed as

Heart FailureAnimalsDisease Models, AnimalHumansMiceMuscle, SkeletalRatsRats, Inbred DahlStroke VolumeAnimal modelsHeart failure with preserved ejection fractionSkeletal muscle

Identifiers

PMID33350094
PMCPMC7835579
OpenAlexW3112454773

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.