Evidence map›Paper›PMID 39715749›Full record

ArticleNature communications2024

Preventing excessive autophagy protects from the pathology of mtDNA mutations in Drosophila melanogaster.

Najla El Fissi, Florian A Rosenberger, Kai Chang, Alissa Wilhalm, Tom Barton-Owen, Fynn M Hansen, Zoe Golder, David Alsina, Anna Wedell, Matthias Mann and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. 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

13 authors.

Najla El FissiDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden.
Florian A Rosenberger *Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Martinsried, 82152, Germany.ORCID 0000-0003-4604-6170
Kai Chang *Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden.
Alissa WilhalmDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden.
Tom Barton-OwenDepartment of Clinical Neurosciences, School of Clinical Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK.
Fynn M HansenProteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Martinsried, 82152, Germany.
Zoe GolderDepartment of Clinical Neurosciences, School of Clinical Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK.
David AlsinaDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden.ORCID 0000-0003-0708-7391
Anna WedellCentre for Inherited Metabolic Diseases, Karolinska University Hospital, 171 76, Stockholm, Sweden.
Matthias MannProteomics and Signal Transduction, Max-Planck Institute of Biochemistry, Martinsried, 82152, Germany.ORCID 0000-0003-1292-4799
Patrick F ChinneryDepartment of Clinical Neurosciences, School of Clinical Medicine, University of Cambridge, Cambridge Biomedical Campus, Cambridge, UK.
Christoph FreyerDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden. christoph.freyer@ki.se.ORCID 0000-0003-0418-1673
Anna WredenbergDepartment of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65, Stockholm, Sweden. anna.wredenberg@ki.se.ORCID 0000-0002-2500-6121

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
European Molecular Biology Organization (EMBO) ALTF 399-2021Karolinska Institutet (Karolinska Institute) 2-190/2022Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) KAW2019.0109Knut och Alice Wallenbergs Stiftelse (Knut and Alice Wallenberg Foundation) KAW2020.0228NIH HHS P40 OD018537Novo Nordisk Fonden (Novo Nordisk Foundation) NN0082202Vetenskapsrådet (Swedish Research Council) 2019-01154Vetenskapsrådet (Swedish Research Council) 2022-01287Vetenskapsrådet (Swedish Research Council) 2023-07091
6 · The paper itself

Abstract

Aberration of mitochondrial function is a shared feature of many human pathologies, characterised by changes in metabolic flux, cellular energetics, morphology, composition, and dynamics of the mitochondrial network. While some of these changes serve as compensatory mechanisms to maintain cellular homeostasis, their chronic activation can permanently affect cellular metabolism and signalling, ultimately impairing cell function. Here, we use a Drosophila melanogaster model expressing a proofreading-deficient mtDNA polymerase (POLγ

Indexed as

AutophagyDNA, MitochondrialDrosophila melanogasterDrosophila ProteinsMutationAnimalsAnimals, Genetically ModifiedMitochondriaMitochondrial DiseasesPhenotypeSirolimusDNA, MitochondrialDrosophila ProteinsSirolimus

Identifiers

PMID39715749
PMCPMC11666730

What OpenQuestion holds

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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.