Evidence mapPaperPMID 40107718Full record

ArticleEuropean journal of heart failure2025

Cardioprotective effects of semaglutide on isolated human ventricular myocardium.

Thomas Krammer, Maria J Baier, Philipp Hegner, Tilman Zschiedrich, David Lukas, Matthias Wolf, Christian Le Phu, Vanessa Lutz, Katja Evert, Kostiantyn Kozakov and 7 more

Abstract read
In one paragraph

Article in European journal of heart failure, 2025. 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
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

12 citing papers in PubMed.

  1. Review
  2. Contractile effects of dulaglutide in the human atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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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

17 authors.

Thomas Krammer *Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Maria J Baier *Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Philipp Hegner *Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Tilman ZschiedrichDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
David LukasDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Matthias WolfDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Christian Le PhuDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Vanessa LutzDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Katja EvertInstitute for Pathology, University of Regensburg, Regensburg, Germany.
Kostiantyn KozakovCardiothoracic Surgery, University Hospital Regensburg, Regensburg, Germany.
Jing LiCardiothoracic Surgery, University Hospital Regensburg, Regensburg, Germany.
Andreas HolzamerCardiothoracic Surgery, University Hospital Regensburg, Regensburg, Germany.
Lars S MaierDepartment of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Zdenek ProvaznikCardiothoracic Surgery, University Hospital Regensburg, Regensburg, Germany.
Donald M BersDepartment of Pharmacology, University of California, Davis, CA, USA.
Stefan Wagner *Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.
Julian Mustroph *Department of Internal Medicine II, University Hospital Regensburg, Regensburg, Germany.ORCID https://orcid.org/0000-0001-9668-7852

Funding

Deutsche Forschungsgemeinschaft HE 10029/1-1Deutsche Forschungsgemeinschaft MA 1982/11-1Deutsche Forschungsgemeinschaft MU 4555/2-1Deutsche Forschungsgemeinschaft MU 4555/5-1Deutsche Forschungsgemeinschaft SFB TR374 TP A6Deutsche Gesellschaft für Kardiologie-Herz und Kreislaufforschung Clinician Scientist ProgramDeutsche Herzstiftung project grantElse Kröner-Fresenius-Stiftung 2023_EKEA.186Else Kröner-Fresenius-Stiftung 2023_EKES.04Reform program, Faculty of Medicine, University of Regensburg
6 · The paper itself

Abstract

aimsSemaglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, has shown promising effects in reducing cardiovascular events in patients with obesity and heart failure (HF) with preserved ejection fraction (HFpEF) irrespective of concomitant diabetes. However, the exact mechanisms underlying its cardioprotective actions remain unclear. Our study investigates the direct effects of semaglutide on human cardiomyocytes, focusing on calcium (Ca) and sodium (Na) handling and its potential to improve myocardial contractility. METHODS AND

resultsHuman left ventricular cardiomyocytes were isolated from non-failing (NF) hearts, patients with aortic stenosis and a HFpEF-like phenotype (AS), and those with end-stage HF with reduced ejection fraction (HFrEF). Late Na current (I

conclusionSemaglutide directly modulates ion homeostasis in human cardiomyocytes, reducing proarrhythmic diastolic SR Ca leak and enhancing systolic function, which may explain its observed clinical benefits. These findings provide mechanistic insights into the cardioprotective effects of semaglutide and suggest its potential therapeutic use in HF.

Indexed as

Glucagon-Like PeptidesHeart FailureHeart VentriclesMyocardial ContractionMyocytes, CardiacPeptide FragmentsAgedCalciumCardiotonic AgentsFemaleGlucagon-Like Peptide 1HumansMaleMiddle AgedSarcoplasmic ReticulumSemaglutideCalciumCardiotonic AgentsGlucagon-Like Peptide 1Glucagon-Like PeptidesPeptide FragmentsSemaglutideCalciumHeart failureHuman cardiomyocytesSemaglutide

Identifiers

PMID40107718
PMCPMC12370581

What Socratic holds

Texttitle and abstract
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.