Evidence map›Paper›PMID 37533404›Full record

ArticleEMBO molecular medicine2023

Metabolic switch from fatty acid oxidation to glycolysis in knock-in mouse model of Barth syndrome.

Arpita Chowdhury, Angela Boshnakovska, Abhishek Aich, Aditi Methi, Ana Maria Vergel Leon, Ivan Silbern, Christian Lüchtenborg, Lukas Cyganek, Jan Prochazka, Radislav Sedlacek and 11 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
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

24 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Cardiolipin preserves TNature metabolism · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  16. Review
  17. Article
  18. What can ATP content tell us about Barth syndrome muscle phenotypes?Journal of translational genetics and genomics · 2025
    Article
  19. A Barth Syndrome Patient-DerivedInternational journal of molecular sciences · 2024
    Article
  20. 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

21 authors at 4 institutions in 2 countries.

Arpita Chowdhury *Department of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.ORCID 0000-0001-5025-0268
Angela Boshnakovska *Department of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.ORCID 0009-0008-3572-0223
Abhishek AichDepartment of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.
Aditi MethiDepartment of Psychiatry and Psychotherapy, University Medical Center Göttingen, Göttingen, Germany.
Ana Maria Vergel LeonDepartment of Cardiovascular Physiology, University Medical Center Göttingen, Göttingen, Germany.
Ivan SilbernThe Bioanalytical Mass Spectrometry Group, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0001-8284-954X
Christian LüchtenborgHeidelberg University Biochemistry Center (BZH), Heidelberg, Germany.
Lukas CyganekCluster of Excellence "Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells" (MBExC), University of Göttingen, Göttingen, Germany.
Jan ProchazkaCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.ORCID 0000-0003-4675-8995
Radislav SedlacekCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.
Jiri LindovskyCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.
Dominic WachsDepartment of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.
Zuzana NichtovaCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.
Dagmar ZudovaCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.
Gizela KoubkovaCzech Centre for Phenogenomics, Institute of Molecular Genetics of the CAS, Prague, Czech Republic.
André FischerCluster of Excellence "Multiscale Bioimaging: from Molecular Machines to Networks of Excitable Cells" (MBExC), University of Göttingen, Göttingen, Germany.
Henning UrlaubThe Bioanalytical Mass Spectrometry Group, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.ORCID 0000-0003-1837-5233
Britta BrüggerHeidelberg University Biochemistry Center (BZH), Heidelberg, Germany.
Dörthe M KatschinskiDepartment of Cardiovascular Physiology, University Medical Center Göttingen, Göttingen, Germany.ORCID 0000-0003-4630-9081
Jan DudekDepartment of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.
Peter RehlingDepartment of Cellular Biochemistry, University Medical Center Göttingen, Göttingen, Germany.ORCID 0000-0001-5661-5272
Universitätsmedizin Göttingen · DECzech Academy of Sciences, Institute of Molecular Genetics · CZGerman Center for Neurodegenerative Diseases · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are central for cellular metabolism and energy supply. Barth syndrome (BTHS) is a severe disorder, due to dysfunction of the mitochondrial cardiolipin acyl transferase tafazzin. Altered cardiolipin remodeling affects mitochondrial inner membrane organization and function of membrane proteins such as transporters and the oxidative phosphorylation (OXPHOS) system. Here, we describe a mouse model that carries a G197V exchange in tafazzin, corresponding to BTHS patients. TAZ

Indexed as

Barth SyndromeAdenosine TriphosphateAMP-Activated Protein KinasesAnimalsCardiolipinsFatty AcidsGlycolysisMiceAdenosine TriphosphateAMP-Activated Protein KinasesCardiolipinsFatty AcidsBarth syndromecardiolipincardiomyopathymitochondriatafazzin

Identifiers

PMID37533404
PMCPMC10493589
OpenAlexW4385514478

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.