Evidence map›Paper›PMID 26050974›Full record

ReviewBiochimica et biophysica acta2015

The role of mitochondrial dysfunction in age-related diseases.

Rebecca K Lane, Tyler Hilsabeck, Shane L Rea

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03800342 (Recovery, Fatigability, and Proteomic Response to Aerobic Exercise Training in Healthy Individuals), which is not on this map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
8.7field-weighted citation impact, top 2% 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.

NCT03800342 nacompletednot on this mapstarted 2019, after this paper: background citation

Recovery, Fatigability, and Proteomic Response to Aerobic Exercise Training in Healthy Individuals

TypeinterventionalSponsorGeorge Mason UniversityRan2019 to 2019Enrolled21ConditionsAdult, FatigueArmsAerobic Exercise Training
3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Role of Mitochondrial Dynamics in Skin Homeostasis: An Update.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Oxidized Low-Density Lipoprotein and Its Role in Immunometabolism.International journal of molecular sciences · 2024
    Review
  18. Article
  19. 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
  20. Article

56 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

3 authors at 1 institution in 1 country.

Rebecca K LaneThe Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA.
Tyler HilsabeckThe Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA; The University of Texas, San Antonio, TX 78249, USA.
Shane L ReaThe Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center, San Antonio, TX 78245, USA; Department of Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA. Electronic address: reas3@uthscsa.edu.
The University of Texas Health Science Center at San Antonio · US

Funding

A 'Mitochondria-nucleus-ribosome' Signaling Axis Controls Lifespan in Mit MutantsR21AG047561 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI REA, SHANE L. · 2014 to 2015
$390k
NIA NIH HHS R21 AG047561NIA NIH HHS R21AG047561
6 · The paper itself

Abstract

The aging process is accompanied by the onset of disease and a general decline in wellness. Insights into the aging process have revealed a number of cellular hallmarks of aging, among these epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and stem cell exhaustion. Mitochondrial dysfunction increasingly appears to be a common factor connecting several of these hallmarks, driving the aging process and afflicting tissues throughout the body. Recent research has uncovered a much more complex involvement of mitochondria in the cell than has previously been appreciated and revealed novel ways in which mitochondrial defects feed into disease pathology. In this review we evaluate ways in which problems in mitochondria contribute to disease beyond the well-known mechanisms of oxidative stress and bioenergetic deficits, and we predict the direction that mitochondrial disease research will take in years to come.

Indexed as

AgingAnimalsAtherosclerosisCell DifferentiationHumansMitochondriaNeurodegenerative DiseasesOsteoporosisStem CellsAgingAtherosclerosisImmunityMitochondriaNeurodegenerationOsteoporosisSirtuinsStem cells

Identifiers

PMID26050974
PMCPMC10481969
OpenAlexW625172625

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.