Evidence map›Paper›PMID 38167524›Full record

ArticleStem cell research & therapy2024

Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation.

Yeranuhi Hovhannisyan, Zhenlin Li, Domitille Callon, Rodolphe Suspène, Vivien Batoumeni, Alexis Canette, Jocelyne Blanc, Hakim Hocini, Cécile Lefebvre, Nora El-Jahrani and 12 more

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Natural History, Phenotype Spectrum, and Clinical Outcomes of Desmin (Circulation. Genomic and precision medicine · 2025
    Pooled it
  2. Article
  3. The R120G knock-in mutation in αB-crystallin is insufficient to induce cardiomyopathy in mice.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  4. CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Generation and applications of cardiac spheroids.npj biomedical innovations · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Natural History, Phenotype Spectrum and Clinical Outcomes of Desmin (medRxiv : the preprint server for health sciences · 2024
    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

22 authors.

Yeranuhi HovhannisyanUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Zhenlin LiUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Domitille CallonUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Rodolphe SuspèneVirus and Cellular Stress Unit, Department of Virology, Institut Pasteur, Université Paris Cité, Paris, France.
Vivien BatoumeniUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Alexis CanetteService de Microscopie Électronique (IBPS-SME), Institut de Biologie Paris-Seine (IBPS), CNRS, Sorbonne Université, Paris, France.
Jocelyne BlancUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Hakim HociniINSERM U955, Equipe 16, Université Paris-Est Créteil, Créteil, France.
Cécile LefebvreINSERM U955, Equipe 16, Université Paris-Est Créteil, Créteil, France.
Nora El-JahraniINSERM U955, Equipe 16, Université Paris-Est Créteil, Créteil, France.
Maria KitsaraUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Aurore L'honoréUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Ekaterini KordeliUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Paul FornesDepartment of Pathology, Academic Hospital of Reims, Reims, France.
Jean-Paul ConcordetINSERM U1154, CNRS UMR7196, Museum National d'Histoire Naturelle, Paris, France.
Gérard TachdjianLaboratoire de Cytogénétique, Service d'Histologie-Embryologie-Cytogénétique, AP-HP, Hôpital Antoine Béclère, Université Paris Saclay, Clamart, France.
Anne-Marie RodriguezUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France.
Jean-Pierre VartanianVirus and Cellular Stress Unit, Department of Virology, Institut Pasteur, Université Paris Cité, Paris, France.
Anthony BéhinReference Center for Muscle Diseases Paris-Est, Myology Institute, AP-HP, Pitié-Salpêtrière Hospital, Sorbonne Université, Paris, France.
Karim WahbiCardiology Department, AP-HP, Cochin Hospital, Université Paris Cité, Paris, France.
Pierre JoanneUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France. pierre.joanne@sorbonne-universite.fr.
Onnik AgbulutUMR CNRS 8256, INSERM U1164, Biological Adaptation and Ageing, Institut de Biologie Paris-Seine (IBPS), Sorbonne Université, 7, Quai St Bernard (case 256), 75005, Paris, France. onnik.agbulut@sorbonne-universite.fr.ORCID 0000-0003-1923-8871

Funding

AFM-Téléthon 20479AFM-Téléthon 22142Agence Nationale de la Recherche ANR-21-CE19-0027Association Nationale de la Recherche et de la Technologie 2020/0074
6 · The paper itself

Abstract

backgroundBeyond the observed alterations in cellular structure and mitochondria, the mechanisms linking rare genetic mutations to the development of heart failure in patients affected by desmin mutations remain unclear due in part, to the lack of relevant human cardiomyocyte models.

methodsTo shed light on the role of mitochondria in these mechanisms, we investigated cardiomyocytes derived from human induced pluripotent stem cells carrying the heterozygous DES

resultsThe heterozygous DES

conclusionsThis work highlights the deleterious effects of DES

Indexed as

CardiomyopathiesInduced Pluripotent Stem CellsDesminHumansMitochondriaMutationMyocytes, CardiacDesminCardiomyocytesDesminDilated cardiomyopathyHeart failureiPSCMitochondriaMyofibrillar myopathyStem cells

Identifiers

PMID38167524
PMCPMC10763022

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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.