Evidence map›Paper›PMID 28432755›Full record

ReviewJournal of cachexia, sarcopenia and muscle2017

Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue.

Kerstin Boengler, Maik Kosiol, Manuel Mayr, Rainer Schulz, Susanne Rohrbach

Registry-linked trialAbstract readReview
In one paragraph

Review in Journal of cachexia, sarcopenia and muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05482711 (Assessment of Fuel Utilization and Circadian Rhythms in Overweight, Older Adults Following Time Restricted Eating - Phase 2), which is not on this map. Cited by 225 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 3 pooled it
–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.

NCT05482711 nacompletednot on this mapstarted 2023, after this paper: background citation

Assessment of Fuel Utilization and Circadian Rhythms in Overweight, Older Adults Following Time Restricted Eating - Phase 2 (FAR Phase 2)

TypeinterventionalSponsorUniversity of FloridaRan2023 to 2026Enrolled15ConditionsAgingArmsTime Restricted Eating Intervention
3 · Its place in the literature

Who cites it

225 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  7. Review
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  9. Article
  10. Article
  11. Review
  12. Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026
    Review
  13. Review
  14. The effect of obesity and aging on NADInternational journal of obesity (2005) · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Leveraging mitochondrial stress to improve healthy aging.Sports medicine and health science · 2026
    Review

165 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

5 authors.

Kerstin BoenglerInstitute of Physiology, Justus Liebig University Giessen, Aulweg 129, 35392, Giessen, Germany.
Maik KosiolInstitute of Physiology, Justus Liebig University Giessen, Aulweg 129, 35392, Giessen, Germany.
Manuel MayrKing's British Heart Foundation Centre, King's College London, 125 Coldharbour Lane, London, SE5 9NU, UK.
Rainer SchulzInstitute of Physiology, Justus Liebig University Giessen, Aulweg 129, 35392, Giessen, Germany.
Susanne RohrbachInstitute of Physiology, Justus Liebig University Giessen, Aulweg 129, 35392, Giessen, Germany.

Funding

British Heart Foundation CH/16/3/32406British Heart Foundation FS/13/2/29892British Heart Foundation RG/16/14/32397
6 · The paper itself

Abstract

Age is the most important risk factor for most diseases. Mitochondria play a central role in bioenergetics and metabolism. In addition, several lines of evidence indicate the impact of mitochondria in lifespan determination and ageing. The best-known hypothesis to explain ageing is the free radical theory, which proposes that cells, organs, and organisms age because they accumulate reactive oxygen species (ROS) damage over time. Mitochondria play a central role as the principle source of intracellular ROS, which are mainly formed at the level of complex I and III of the respiratory chain. Dysfunctional mitochondria generating less ATP have been observed in various aged organs. Mitochondrial dysfunction comprises different features including reduced mitochondrial content, altered mitochondrial morphology, reduced activity of the complexes of the electron transport chain, opening of the mitochondrial permeability transition pore, and increased ROS formation. Furthermore, abnormalities in mitochondrial quality control or defects in mitochondrial dynamics have also been linked to senescence. Among the tissues affected by mitochondrial dysfunction are those with a high-energy demand and thus high mitochondrial content. Therefore, the present review focuses on the impact of mitochondria in the ageing process of heart and skeletal muscle. In this article, we review different aspects of mitochondrial dysfunction and discuss potential therapeutic strategies to improve mitochondrial function. Finally, novel aspects of adipose tissue biology and their involvement in the ageing process are discussed.

Indexed as

Adipose TissueAge FactorsAgingAnimalsHumansMitochondriaMitochondrial DynamicsMuscle, SkeletalMyocardiumOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen SpeciesAgeingCaloric restrictionHeartMitochondriaReactive oxygen speciesSkeletal muscle

Identifiers

PMID28432755
PMCPMC5476857

What OpenQuestion holds

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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.