Evidence map›Paper›PMID 31132524›Full record

ArticleRedox biology2019

Functional wiring of proteostatic and mitostatic modules ensures transient organismal survival during imbalanced mitochondrial dynamics.

Sentiljana Gumeni, Zoi Evangelakou, Eleni N Tsakiri, Luca Scorrano, Ioannis P Trougakos

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
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  4. Studying Cellular Senescence Using the Model Organism Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2025
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  6. Review
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  11. Toward a Consensus in the Repertoire of Hemocytes Identified inFrontiers in cell and developmental biology · 2021
    Article
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  13. Review
  14. Article
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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

5 authors at 2 institutions in 2 countries.

Sentiljana GumeniDepartment of Cell Biology and Biophysics, Faculty of Biology, National & Kapodistrian University of Athens, 15784, Greece.
Zoi EvangelakouDepartment of Cell Biology and Biophysics, Faculty of Biology, National & Kapodistrian University of Athens, 15784, Greece.
Eleni N TsakiriDepartment of Cell Biology and Biophysics, Faculty of Biology, National & Kapodistrian University of Athens, 15784, Greece.
Luca ScorranoDulbecco-Telethon Institute, Venetian Institute of Molecular Medicine and Department of Biology, University of Padua, Padova, 35129, Italy.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National & Kapodistrian University of Athens, 15784, Greece. Electronic address: itrougakos@biol.uoa.gr.
National and Kapodistrian University of Athens · GRUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Being an assembly of protein machines, cells depend on adequate supply of energetic molecules for retaining their homeodynamics. Consequently, mitochondria functionality is ensured by quality control systems and mitochondrial dynamics (fusion/fission). Similarly, proteome stability is maintained by the machineries of the proteostasis network. We report here that reduced mitochondrial fusion rates in Drosophila caused developmental lethality or if induced in the adult accelerated aging. Imbalanced mitochondrial dynamics were tolerable for various periods in young flies, where they caused oxidative stress and proteome instability that mobilized Nrf2 and foxo to upregulate cytoprotective antioxidant/proteostatic modules. Consistently, proteasome inhibition or Nrf2, foxo knock down in young flies exaggerated perturbed mitochondrial dynamics toxicity. Neither Nrf2 overexpression (with concomitant proteasome activation) nor Atg8a upregulation suppressed the deregulated mitochondrial dynamics toxicity, which was mildly mitigated by antioxidants. Thus, despite extensive functional wiring of mitostatic and antioxidant/proteostatic modules, sustained loss-of mitostasis exhausts adaptation responses triggering premature aging.

Indexed as

Mitochondrial DynamicsProteostasisAgingAnimalsAnimals, Genetically ModifiedAntioxidantsDrosophila melanogasterDrosophila ProteinsEnergy MetabolismFemaleGenes, LethalMaleMitochondriaMitochondrial ProteinsOxidative StressProteomeAntioxidantsDrosophila ProteinsMitochondrial ProteinsProteomeAgingDrp1MitofusinsMitostasisOpa1Proteostasis

Identifiers

PMID31132524
PMCPMC6536731
OpenAlexW2945878840

What OpenQuestion holds

Textmetadata
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.