Evidence map›Paper›PMID 35820914›Full record

ArticleBMC biology2022

Antagonistic effects of mitochondrial matrix and intermembrane space proteases on yeast aging.

Montserrat Vega, David Castillo, Laura de Cubas, Yirong Wang, Ying Huang, Elena Hidalgo, Margarita Cabrera

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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  5. Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025
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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

7 authors at 2 institutions in 2 countries.

Montserrat VegaOxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, C/ Dr. Aiguader 88, 08003, Barcelona, Spain.
David CastilloBatchX Inc, San Jose, CA, USA.
Laura de CubasOxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, C/ Dr. Aiguader 88, 08003, Barcelona, Spain.
Yirong WangJiangsu Key Laboratory for Microbes and Genomics, School of Life Sciences, Nanjing Normal University, 1 Wenyuan Road, Nanjing, 210023, China.
Ying HuangJiangsu Key Laboratory for Microbes and Genomics, School of Life Sciences, Nanjing Normal University, 1 Wenyuan Road, Nanjing, 210023, China.
Elena HidalgoOxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, C/ Dr. Aiguader 88, 08003, Barcelona, Spain.
Margarita CabreraOxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, C/ Dr. Aiguader 88, 08003, Barcelona, Spain. mcabrera@cbm.csic.es.ORCID 0000-0002-2978-8255
Universitat Pompeu Fabra · ESNanjing Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn many organisms, aging is characterized by a loss of mitochondrial homeostasis. Multiple factors such as respiratory metabolism, mitochondrial fusion/fission, or mitophagy have been linked to cell longevity, but the exact impact of each one on the aging process is still unclear.

resultsUsing the deletion mutant collection of the fission yeast Schizosaccharomyces pombe, we have developed a genome-wide screening for mutants with altered chronological lifespan. We have identified four mutants associated with proteolysis at the mitochondria that exhibit opposite effects on longevity. The analysis of the respiratory activity of these mutants revealed a positive correlation between increased respiration rate and prolonged lifespan. We also found that the phenotype of the long-lived protease mutants could not be explained by impaired mitochondrial fusion/fission activities, but it was dependent on mitophagy induction. The anti-aging role of mitophagy was supported by the effect of a mutant defective in degradation of mitochondria, which shortened lifespan of the long-lived mutants.

conclusionsOur characterization of the mitochondrial protease mutants demonstrates that mitophagy sustains the lifespan extension of long-lived mutants displaying a higher respiration potential.

Indexed as

Saccharomyces cerevisiae ProteinsSchizosaccharomycesMitochondriaMitochondrial DynamicsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsChronological agingMitochondrial dynamicsMitophagyMitoproteasesRespiratory capacity

Identifiers

PMID35820914
PMCPMC9277893
OpenAlexW4285088996

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.