Evidence map›Paper›PMID 25546256›Full record

ArticleProteomics2015

Proteomic analysis and functional characterization of mouse brain mitochondria during aging reveal alterations in energy metabolism.

Kelly L Stauch, Phillip R Purnell, Lance M Villeneuve, Howard S Fox

Open access · greenAbstract read
In one paragraph

Article in Proteomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. A scoping review of computational models on human glucose cerebral metabolism.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Review
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  11. Mitophagy and the Brain.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Mitoproteomics: Tackling Mitochondrial Dysfunction in Human Disease.Oxidative medicine and cellular longevity · 2018
    Review
  20. Of Energy and Entropy: The Ineluctable Impact of Aging in Old Age Dementia.International journal of molecular sciences · 2017
    Review
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.

Kelly L StauchDepartment of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, USA.
Phillip R Purnell
Lance M Villeneuve
Howard S Fox
University of Nebraska Medical Center · US

Funding

Therapeutics Core (Page 286)P30MH062261 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E · 2000 to 2021
$37.7M
Molecular Aspects of CNS Dysfunction Due to SIV/HIVR01MH073490 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI FOX, HOWARD S · 2005 to 2014
$3.9M
NIMH NIH HHS P30 MH06221NIMH NIH HHS P30 MH062261NIMH NIH HHS R01 MH073490
6 · The paper itself

Abstract

Mitochondria are the main cellular source of reactive oxygen species and are recognized as key players in several age-associated disorders and neurodegeneration. Their dysfunction has also been linked to cellular aging. Additionally, mechanisms leading to the preservation of mitochondrial function promote longevity. In this study we investigated the proteomic and functional alterations in brain mitochondria isolated from mature (5 months old), old (12 months old), and aged (24 months old) mice as determinants of normal "healthy" aging. Here the global changes concomitant with aging in the mitochondrial proteome of mouse brain analyzed by quantitative mass-spectrometry based super-SILAC identified differentially expressed proteins involved in several metabolic pathways including glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation. Despite these changes, the bioenergetic function of these mitochondria was preserved. Overall, this data indicates that proteomic changes during aging may compensate for functional defects aiding in preservation of mitochondrial function. The mass spectrometry proteomics data have been deposited to the ProteomeXchange Consortium with the data set identifier PXD001370 (http://proteomecentral.proteomexchange.org/dataset/PXD001370).

Indexed as

AgingEnergy MetabolismAnimalsBrainMiceMice, Inbred C57BLMitochondriaMitochondrial ProteinsProtein Interaction MapsProteomeProteomicsTandem Mass SpectrometryTranscriptional ActivationMitochondrial ProteinsProteomeAgingBioenergeticsBrain mitochondriaQuantitative proteomics

Identifiers

PMID25546256
PMCPMC4465935
OpenAlexW2122978806

What OpenQuestion holds

Textmetadata
LicenceTDM
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.