Evidence map›Paper›PMID 25601284›Full record

ArticleScientific reports2015

Simultaneous impairment of mitochondrial fission and fusion reduces mitophagy and shortens replicative lifespan.

Dominik Bernhardt, Matthias Müller, Andreas S Reichert, Heinz D Osiewacz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 119 citations in OpenAlex.

  1. Proceedings of the National Academy of Sciences of the United States of America · 2026
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  8. De NovoInternational journal of molecular sciences · 2025
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12 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Dominik BernhardtGoethe University, Faculty for Biosciences &Cluster of Excellence, 'Macromolecular Complexes' Frankfurt, Institute of Molecular Biosciences, Max-von-Laue-Str. 9, 60438 Frankfurt, Germany.
Matthias MüllerMitochondrial Biology, Buchmann Institute for Molecular Life Sciences &Zentrum für Molekulare Medizin, Goethe University, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany.
Andreas S Reichert1] Mitochondrial Biology, Buchmann Institute for Molecular Life Sciences &Zentrum für Molekulare Medizin, Goethe University, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany [2] Heinrich-Heine Universität, Universitätsklinikum Düsseldorf, Institut für Biochemie und Molekularbiologie I, Universitätsstr. 1, 40225 Düsseldorf.
Heinz D OsiewaczGoethe University, Faculty for Biosciences &Cluster of Excellence, 'Macromolecular Complexes' Frankfurt, Institute of Molecular Biosciences, Max-von-Laue-Str. 9, 60438 Frankfurt, Germany.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging of biological systems is accompanied by degeneration of mitochondrial functions. Different pathways are active to counteract the processes which lead to mitochondrial dysfunction. Mitochondrial dynamics, the fission and fusion of mitochondria, is one of these quality control pathways. Mitophagy, the controlled degradation of mitochondria, is another one. Here we show that these pathways are linked. A double deletion mutant of Saccharomyces cerevisiae in which two essential components of the fission and fusion machinery, Dnm1 and Mgm1, are simultaneously ablated, contain wild-type like filamentous mitochondria, but are characterized by impaired respiration, an increased sensitivity to different stressors, increased mitochondrial protein carbonylation, and a decrease in mitophagy and replicative lifespan. These data show that a balanced mitochondrial dynamics and not a filamentous mitochondrial morphotype per se is the key for a long lifespan and demonstrate a cross-talk between two different mitochondrial quality control pathways.

Indexed as

AutophagyCellular SenescenceGTP-Binding ProteinsGTP PhosphohydrolasesMitochondriaMitochondrial DynamicsMitochondrial ProteinsMitophagySaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNM1 protein, S cerevisiaeGTP-Binding ProteinsGTP PhosphohydrolasesMGM1 protein, S cerevisiaeMitochondrial ProteinsSaccharomyces cerevisiae Proteins

Identifiers

PMID25601284
PMCPMC4298727
OpenAlexW2090633127

What OpenQuestion holds

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LicenceCC BY-NC-ND
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 OpenQuestion graph.