Evidence map›Paper›PMID 41161319›Full record

ArticleCell reports methods2025

A transmission electron microscopy platform for assessing mitochondrial and nuclear architecture in cardiomyocytes.

Mara Kiessling, Juergen Gindlhuber, Amalia Sintou, Ingrid Matzer, Snježana Radulović, Viktoria Trummer-Herbst, Andonita Ajdari, Julia Voglhuber-Höller, Michael Holzer, Tristan A Rodriguez and 5 more

Abstract read
In one paragraph

Article in Cell reports methods, 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. Article
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

15 authors.

Mara KiesslingUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Juergen GindlhuberUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Amalia SintouNational Heart and Lung Institute (NHLI), Imperial College London, London, UK.
Ingrid MatzerUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Snježana RadulovićDivision of Cell Biology, Histology and Embryology, Gottfried Schatz Research Center, Medical University of Graz, Graz, Austria.
Viktoria Trummer-HerbstUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Andonita AjdariUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Julia Voglhuber-HöllerUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Michael HolzerDivision of Pharmacology, Otto-Loewi Research Center, Medical University of Graz, Graz, Austria.
Tristan A RodriguezNational Heart and Lung Institute (NHLI), Imperial College London, London, UK.
Gerd LeitingerDivision of Cell Biology, Histology and Embryology, Gottfried Schatz Research Center, Medical University of Graz, Graz, Austria.
Andreas ZirlikUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria.
Donald M BersDepartment of Pharmacology, University of California, Davis, Davis, CA, USA.
Susanne SattlerUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria; National Heart and Lung Institute (NHLI), Imperial College London, London, UK; Division of Pharmacology, Otto-Loewi Research Center, Medical University of Graz, Graz, Austria. Electronic address: susanne.sattler@medunigraz.at.
Senka Ljubojevic-HolzerUniversity Heart Center Graz, Division of Cardiology, Medical University of Graz, Graz, Austria; Gottfried Schatz Research Center, Medical University of Graz, Graz, Austria; BioTechMed-Graz, Graz, Austria. Electronic address: senka.ljubojevic@medunigraz.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are central to cardiomyocyte function, and their spatial organization regulates nuclear signaling and gene transcription, holding potential for novel cardioprotective interventions. We developed a transmission electron microscopy platform optimized for resolving mitochondrial subpopulations and nuclear architecture in adult cardiomyocytes. This approach reliably captures longitudinal sections containing the center of the nucleus and perinuclear regions, enabling consistent imaging of subcellular nanostructures, assessment of pharmacological effects within the same organism, and visualization of extracellular vesicles carrying dysfunctional mitochondria. Integrated with an analysis workflow employing machine learning-based segmentation for annotation, the method allows automated quantification of mitochondrial and nuclear architecture and positioning. Using Drp1-deficient mice with impaired mitochondrial fission, we demonstrate this tool's ability to uncover nanoscale remodeling of mitochondria and nuclei under stress. Our platform overcomes challenges in electron microscopy analysis, providing a powerful resource to interrogate mitochondrial-nuclear dynamics in cardiac (patho)physiology. These insights will inform therapeutic targeting of bioenergetic failure.

Indexed as

Cell NucleusMicroscopy, Electron, TransmissionMitochondriaMitochondria, HeartMyocytes, CardiacAnimalsDynaminsMiceMice, Inbred C57BLMitochondrial DynamicsDynaminsautomated image analysiscardiomyocyteCP: cell biologyCP: imagingcristae densitymorphometric analysisnucleusorganelle interactionsperinuclear mitochondriasubcellular imagingtransmission electron microscopyultrastructure analysis

Identifiers

PMID41161319
PMCPMC12664883

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.