Evidence map›Paper›PMID 40649974›Full record

ArticleInternational journal of molecular sciences2025

Skeletal Muscle Alterations in Different Phenotypes of Heart Failure with Preserved Ejection Fraction.

Beatrice Vahle, Romy Klädtke, Antje Schauer, T Scott Bowen, Ulrik Wisløff, Axel Linke, Volker Adams

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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.

Beatrice VahleLaboratory of Molecular and Experimental Cardiology, University Clinic, Department of Internal Medicine, Heart Center, University of Technology Dresden, 01307 Dresden, Germany.ORCID 0009-0000-8110-1943
Romy KlädtkeLaboratory of Molecular and Experimental Cardiology, University Clinic, Department of Internal Medicine, Heart Center, University of Technology Dresden, 01307 Dresden, Germany.
Antje SchauerLaboratory of Molecular and Experimental Cardiology, University Clinic, Department of Internal Medicine, Heart Center, University of Technology Dresden, 01307 Dresden, Germany.
T Scott BowenSchool of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK.ORCID 0000-0002-1740-2474
Ulrik WisløffCardiac Exercise Research Group (CERG), Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, 7006 Trondheim, Norway.ORCID 0000-0002-7211-3587
Axel LinkeLaboratory of Molecular and Experimental Cardiology, University Clinic, Department of Internal Medicine, Heart Center, University of Technology Dresden, 01307 Dresden, Germany.
Volker AdamsLaboratory of Molecular and Experimental Cardiology, University Clinic, Department of Internal Medicine, Heart Center, University of Technology Dresden, 01307 Dresden, Germany.ORCID 0000-0002-7955-7324

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure with preserved ejection fraction (HFpEF) shows diverse disease patterns, with various combinations of comorbidities and symptoms. A common hallmark is exercise intolerance, caused by alterations in the peripheral skeletal muscle (SKM) including a recently indicated titin hyperphosphorylation. Our aim is to compare a metabolic syndrome- (ZSF-1 rats) and a hypertension-driven (Dahl salt-sensitive (DSS) rats) HFpEF rat-model in relation to SKM function and titin phosphorylation. Obese ZSF-1 and high-salt fed DSS rats (HFpEF) were compared to lean ZSF-1 and low-salt fed rats (con). HFpEF was confirmed by echocardiography and invasive haemodynamic measurements. SKM atrophy, in vitro force measurements, titin- and contractile protein expression were evaluated. Obese ZSF-1 HFpEF rats showed muscle atrophy, reduced muscle force and increased titin phosphorylation compared to controls, which was not detected in hypertensive DSS rats. Fiber type specific troponins, myostatin and four and a half LIM domain 1 were differently regulated between the two models. Altogether, our results show that both animal models of HFpEF exhibit different SKM phenotypes, probably based on the divergent disease etiologies, which may help to define the most suitable animal model for HFpEF to test potential treatment regimens.

Indexed as

Heart FailureMuscle, SkeletalStroke VolumeAnimalsConnectinDisease Models, AnimalHypertensionMaleMetabolic SyndromeMuscular AtrophyObesityPhenotypePhosphorylationRatsRats, Inbred DahlConnectinTtn protein, ratDahl salt-sensitive ratsheart failure with preserved ejection fractionHFpEFskeletal muscletitinZSF-1 rats

Identifiers

PMID40649974
PMCPMC12249543

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.