Evidence map›Paper›PMID 40251632›Full record

ArticleStem cell research & therapy2025

Inhibition of ceramide synthesis improves the outcome of ischemia/reperfusion injury in cardiomyocytes derived from human induced pluripotent stem cell.

Pellumb Haxhikadrija, Jasmine M F Wu, Sascha Hübner, Katja Grün, Tom Kretzschmar, Tina Müller, Markus H Gräler, Claudia Backsch, Anja Weise, Elisabeth Klein and 2 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Ceramide as a Biomarker for HFpEF in Women: Menopause, Aging, and Pregnancy.International journal of molecular sciences · 2025
    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

12 authors.

Pellumb HaxhikadrijaDepartment of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Jasmine M F WuDepartment of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Sascha HübnerDepartment of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Katja GrünDepartment of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Tom KretzschmarDepartment of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Tina MüllerDepartment of Anesthesiology and Intensive Care Medicine, Center for Molecular Biomedicine (CMB), University Hospital Jena, Friedrich-Schiller-University, Jena, Germany.
Markus H GrälerDepartment of Anesthesiology and Intensive Care Medicine, Center for Molecular Biomedicine (CMB), University Hospital Jena, Friedrich-Schiller-University, Jena, Germany.
Claudia BackschDepartment of Gynecology and Reproductive Medicine, Jena University Hospital Jena, Friedrich-Schiller-University, Jena, Germany.
Anja WeiseInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
Elisabeth KleinInstitute of Human Genetics, Jena University Hospital, Friedrich Schiller University, Jena, Germany.
P Christian Schulze *Department of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany.
Mohamed M Bekhite *Department of Internal Medicine I, Division of Cardiology, University Hospital Jena, Friedrich-Schiller-University, Am Klinikum 1, 07747, Jena, Germany. Mohamed.el_Saied@med.uni-jena.de.ORCID http://orcid.org/0000-0003-0346-9181

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCeramides are bioactive sphingolipids that have physiological effects on inflammation, apoptosis, and mitochondrial dysfunction. They may play a critical role in the harm of ischemia/reperfusion (IR). Ceramides and IR injury are not well-studied, and there is a lack of human data. METHODS AND

resultsCurrent studies aimed to investigate the role of ceramide buildup in cardiomyocytes (CMs) death using CMs derived from human induced pluripotent stem cell (hiPSC) as a model for simulating IR injury in vitro. In our model, serum- and glucose-free media was used to expose hiPSC-derived CMs to hypoxia (3% O

conclusionsResults from both in vitro and in vivo experiments show that ceramides have a significant role in either mediating or inducing damage to CMs. Additionally, in vitro findings show that ceramide reduction improves the outcome of IR injury by lowering intracellular Ca

Indexed as

CeramidesInduced Pluripotent Stem CellsMyocardial Reperfusion InjuryMyocytes, CardiacReperfusion InjuryAnimalsApoptosisFumonisinsHumansMiceMitochondriaCeramidesFumonisins

Identifiers

PMID40251632
PMCPMC12008854

What OpenQuestion holds

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LicenceCC BY
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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.