Evidence map›Paper›PMID 28986697›Full record

ReviewEuropean journal of applied physiology2018

Targeting mitochondrial function and proteostasis to mitigate dynapenia.

Robert V Musci, Karyn L Hamilton, Benjamin F Miller

Abstract readReview
In one paragraph

Review in European journal of applied physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Exercise sustains the hallmarks of health.Journal of sport and health science · 2023
    Review
  10. Ubiquitin Ligases in Longevity and Aging Skeletal Muscle.International journal of molecular sciences · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Impaired Mitochondrial Energetics Characterize Poor Early Recovery of Muscle Mass Following Hind Limb Unloading in Old Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    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

3 authors.

Robert V MusciTranslational Research on Aging and Chronic Disease Laboratory, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, 80523-1582, USA.
Karyn L Hamilton *Translational Research on Aging and Chronic Disease Laboratory, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, 80523-1582, USA.
Benjamin F Miller *Translational Research on Aging and Chronic Disease Laboratory, Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, 80523-1582, USA. Benjamin.f.miller@colostate.edu.

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Paul S. Maclean · 1995 to 2026
$32.6M
Translational mechanisms of mitochondrial protein synthesisR01AG042569 · NIA · COLORADO STATE UNIVERSITY · PI HAMILTON, KARYN L, MILLER, BENJAMIN FRANCIS · 2013 to 2017
$1.5M
NIA NIH HHS R01 AG042569NIDDK NIH HHS P30 DK048520
6 · The paper itself

Abstract

Traditionally, interventions to treat skeletal muscle aging have largely targeted sarcopenia-the age-related loss of skeletal muscle mass. Dynapenia refers to the age-related loss in skeletal muscle function due to factors outside of muscle mass, which helps to inform treatment strategies for aging skeletal muscle. There is evidence that mechanisms to maintain protein homeostasis and proteostasis, deteriorate with age. One key mechanism to maintain proteostasis is protein turnover, which is an energetically costly process. When there is a mismatch between cellular energy demands and energy provision, inelastic processes related to metabolism are maintained, but there is competition for the remaining energy between the elastic processes of somatic maintenance and growth. With aging, mitochondrial dysfunction reduces ATP generation capacity, constraining the instantaneous supply of energy, thus compromising growth and somatic maintenance processes. Further, with age the need for somatic maintenance increases because of the accumulation of protein damage. In this review, we highlight the significant role mitochondria have in maintaining skeletal muscle proteostasis through increased energy provision, protein turnover, and substrate flux. In addition, we provide evidence that improving mitochondrial function could promote a cellular environment that is conducive to somatic maintenance, and consequently for mitigating dynapenia. Finally, we highlight interventions, such as aerobic exercise, that could be used to improve mitochondrial function and improve outcomes related to dynapenia.

Indexed as

Muscle ContractionProteostasisAnimalsExerciseHumansMitochondria, MuscleMuscle, SkeletalAgingDynapeniaMitochondriaProteostasis

Identifiers

PMID28986697
PMCPMC5756099

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.