Evidence map›Paper›PMID 24815183›Full record

ArticleNature communications2014

Low abundance of the matrix arm of complex I in mitochondria predicts longevity in mice.

Satomi Miwa, Howsun Jow, Karen Baty, Amy Johnson, Rafal Czapiewski, Gabriele Saretzki, Achim Treumann, Thomas von Zglinicki

Abstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing 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

117 citing papers in PubMed.

  1. Article
  2. Review
  3. Changes in the brain [NADFrontiers in aging neuroscience · 2026
    Review
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  6. Review
  7. Aging · 2025
    Article
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  9. Article
  10. Review
  11. Article
  12. Dynamic Changes in Gene Expression Through Aging inbioRxiv : the preprint server for biology · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

57 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

8 authors.

Satomi MiwaInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Howsun JowCentre for Integrated Systems Biology of Ageing and Nutrition, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Karen BatyNewcastle University Protein and Proteome Analysis, Devonshire Building, Devonshire Terrace, Newcastle upon Tyne NE1 7RU, UK.
Amy JohnsonInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Rafal CzapiewskiInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Gabriele SaretzkiInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.
Achim TreumannNewcastle University Protein and Proteome Analysis, Devonshire Building, Devonshire Terrace, Newcastle upon Tyne NE1 7RU, UK.
Thomas von ZglinickiInstitute for Ageing and Health, Newcastle University, Newcastle upon Tyne NE4 5PL, UK.

Funding

Biotechnology and Biological Sciences Research Council BB/C008200/1Biotechnology and Biological Sciences Research Council BB/F010966/1Biotechnology and Biological Sciences Research Council BB/I020748/1
6 · The paper itself

Abstract

Mitochondrial function is an important determinant of the ageing process; however, the mitochondrial properties that enable longevity are not well understood. Here we show that optimal assembly of mitochondrial complex I predicts longevity in mice. Using an unbiased high-coverage high-confidence approach, we demonstrate that electron transport chain proteins, especially the matrix arm subunits of complex I, are decreased in young long-living mice, which is associated with improved complex I assembly, higher complex I-linked state 3 oxygen consumption rates and decreased superoxide production, whereas the opposite is seen in old mice. Disruption of complex I assembly reduces oxidative metabolism with concomitant increase in mitochondrial superoxide production. This is rescued by knockdown of the mitochondrial chaperone, prohibitin. Disrupted complex I assembly causes premature senescence in primary cells. We propose that lower abundance of free catalytic complex I components supports complex I assembly, efficacy of substrate utilization and minimal ROS production, enabling enhanced longevity.

Indexed as

AgingAging, PrematureAnimalsCell LineElectron Transport Complex IHeLa CellsHumansLiverLongevityMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaNADH DehydrogenaseOxidation-ReductionElectron Transport Complex INADH DehydrogenaseNDUFB9 protein, humanNDUFS3 protein, humanProhibitinsReactive Oxygen SpeciesRepressor ProteinsRNA, Small Interfering

Identifiers

PMID24815183
PMCPMC4024759

What OpenQuestion holds

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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.