Evidence map›Paper›PMID 34068411›Full record

ReviewInternational journal of molecular sciences2021

Mitochondrial Bioenergetics and Turnover during Chronic Muscle Disuse.

Jonathan M Memme, Mikhaela Slavin, Neushaw Moradi, David A Hood

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. PROKR1-CREB-NR4A2 axis for oxidative muscle fiber specification and improvement of metabolic function.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. The two faces of mitochondrial CaJournal of physiology and biochemistry · 2026
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Skeletal MuscleDiagnostics (Basel, Switzerland) · 2025
    Article
  13. Article
  14. Adverse Outcome Pathways Applied to Space Radiation Research.Environmental and molecular mutagenesis · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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.

Jonathan M MemmeMuscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada.ORCID 0000-0002-6192-4122
Mikhaela SlavinMuscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada.ORCID 0000-0003-0709-4305
Neushaw MoradiMuscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada.ORCID 0000-0002-6453-0794
David A HoodMuscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada.ORCID 0000-0002-9553-152X
York University · CA

Funding

Natural Sciences and Engineering Research Council of Canada 38462
6 · The paper itself

Abstract

Periods of muscle disuse promote marked mitochondrial alterations that contribute to the impaired metabolic health and degree of atrophy in the muscle. Thus, understanding the molecular underpinnings of muscle mitochondrial decline with prolonged inactivity is of considerable interest. There are translational applications to patients subjected to limb immobilization following injury, illness-induced bed rest, neuropathies, and even microgravity. Studies in these patients, as well as on various pre-clinical rodent models have elucidated the pathways involved in mitochondrial quality control, such as mitochondrial biogenesis, mitophagy, fission and fusion, and the corresponding mitochondrial derangements that underlie the muscle atrophy that ensues from inactivity. Defective organelles display altered respiratory function concurrent with increased accumulation of reactive oxygen species, which exacerbate myofiber atrophy via degradative pathways. The preservation of muscle quality and function is critical for maintaining mobility throughout the lifespan, and for the prevention of inactivity-related diseases. Exercise training is effective in preserving muscle mass by promoting favourable mitochondrial adaptations that offset the mitochondrial dysfunction, which contributes to the declines in muscle and whole-body metabolic health. This highlights the need for further investigation of the mechanisms in which mitochondria contribute to disuse-induced atrophy, as well as the specific molecular targets that can be exploited therapeutically.

Indexed as

Energy MetabolismOrganelle BiogenesisAnimalsHumansMitochondria, MuscleMuscle, SkeletalMuscular Atrophyapoptosisautophagymitochondrial biogenesismitochondrial quality controlmitophagymuscle disusereactive oxygen speciesskeletal muscle atrophy

Identifiers

PMID34068411
PMCPMC8153634
OpenAlexW3163820360

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.