Evidence map›Paper›PMID 25447815›Full record

ReviewArchives of biochemistry and biophysics2015

Mitochondrial maintenance failure in aging and role of sexual dimorphism.

John Tower

Abstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

50 citing papers in PubMed, 69 citations in OpenAlex.

  1. Gender-specific gene profiling inIBRO neuroscience reports · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Mitochondria, Sex, and Cardiovascular Disease: A Complex Interplay.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. The role of mitochondria in sex- and age-specific gene expression in a species without sex chromosomes.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Markers and mechanisms of death inFrontiers in aging · 2023
    Article
  14. Loss of mitochondrial membrane potential (ΔΨJournal of leukocyte biology · 2022
    Article
  15. Article
  16. microPublication biology · 2022
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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

1 author at 1 institution in 1 country.

John TowerMolecular and Computational Biology Program, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089-2910, United States. Electronic address: jtower@usc.edu.
University of Southern California · US

Funding

Translational Research Support CoreP30ES007048 · NIEHS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Joseph Leo Wiemels · 1996 to 2026
$46.4M
AGING-SPECIFIC GENE EXPRESSION IN DROSOPHILAR01AG011833 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI TOWER, JOHN GERARD · 1994 to 2013
$2.8M
NIA NIH HHS AG011833NIA NIH HHS R01 AG011833NIEHS NIH HHS 5P30ES007048NIEHS NIH HHS P30 ES007048
6 · The paper itself

Abstract

Gene expression changes during aging are partly conserved across species, and suggest that oxidative stress, inflammation and proteotoxicity result from mitochondrial malfunction and abnormal mitochondrial-nuclear signaling. Mitochondrial maintenance failure may result from trade-offs between mitochondrial turnover versus growth and reproduction, sexual antagonistic pleiotropy and genetic conflicts resulting from uni-parental mitochondrial transmission, as well as mitochondrial and nuclear mutations and loss of epigenetic regulation. Aging phenotypes and interventions are often sex-specific, indicating that both male and female sexual differentiation promote mitochondrial failure and aging. Studies in mammals and invertebrates implicate autophagy, apoptosis, AKT, PARP, p53 and FOXO in mediating sex-specific differences in stress resistance and aging. The data support a model where the genes Sxl in Drosophila, sdc-2 in Caenorhabditis elegans, and Xist in mammals regulate mitochondrial maintenance across generations and in aging. Several interventions that increase life span cause a mitochondrial unfolded protein response (UPRmt), and UPRmt is also observed during normal aging, indicating hormesis. The UPRmt may increase life span by stimulating mitochondrial turnover through autophagy, and/or by inhibiting the production of hormones and toxic metabolites. The data suggest that metazoan life span interventions may act through a common hormesis mechanism involving liver UPRmt, mitochondrial maintenance and sexual differentiation.

Indexed as

AgingGene Expression RegulationSex CharacteristicsAnimalsAutophagyEpigenesis, GeneticHumansLongevityMitochondriaUnfolded Protein ResponseDosage compensationHeteroplasmyMother’s curseSexual antagonistic pleiotropySexual conflictUPRmt

Identifiers

PMID25447815
PMCPMC4409928
OpenAlexW1990363078

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.