Evidence map›Paper›PMID 26869683›Full record

ArticlePhysiological reports2016

PGC-1α promotes exercise-induced autophagy in mouse skeletal muscle.

Jens F Halling, Stine Ringholm, Maja M Nielsen, Peter Overby, Henriette Pilegaard

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
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  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The Role of PGC1α in Alzheimer's Disease and Therapeutic Interventions.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Aging, Osteo-Sarcopenia, and Musculoskeletal Mechano-Transduction.Frontiers in rehabilitation sciences · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Acute High-Intensity Exercise Impairs Skeletal Muscle Respiratory Capacity.Medicine and science in sports and exercise · 2018
    Article
  19. PGC-1α in exercise and fasting-induced regulation of hepatic UPR in mice.Pflugers Archiv : European journal of physiology · 2018
    Article
  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

5 authors at 1 institution in 1 country.

Jens F HallingDepartment of Biology, Centre of Inflammation and Metabolism, University of Copenhagen, Copenhagen, Denmark.
Stine RingholmDepartment of Biology, Centre of Inflammation and Metabolism, University of Copenhagen, Copenhagen, Denmark.
Maja M NielsenDepartment of Biology, Centre of Inflammation and Metabolism, University of Copenhagen, Copenhagen, Denmark.
Peter OverbyDepartment of Biology, Centre of Inflammation and Metabolism, University of Copenhagen, Copenhagen, Denmark.
Henriette PilegaardDepartment of Biology, Centre of Inflammation and Metabolism, University of Copenhagen, Copenhagen, Denmark hpilegaard@bio.ku.dk.
University of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence suggests that exercise stimulates the degradation of cellular components in skeletal muscle through activation of autophagy, but the time course of the autophagy response during recovery from exercise has not been determined. Furthermore, the regulatory mechanisms behind exercise-induced autophagy remain unclear, although the muscle oxidative phenotype has been linked with basal autophagy levels. Therefore, the aim of this study was to investigate the role of the key regulator of muscle oxidative capacity, PGC-1α, in exercise-induced autophagy at several time points during recovery. Mice with transgenic muscle-specific overexpression (TG) or knockout (MKO) of PGC-1α and their respective littermate controls were subjected to a single 1 h bout of treadmill running and euthanized immediately (0 h), 2, 6, and 10 h after exercise. In the PGC-1α MKO strain, quadriceps protein content of the autophagy marker LC3II was increased from 2 h into recovery in lox/lox control, but not in MKO mice. In the PGC-1α TG strain, quadriceps protein content of LC3II was increased from 2 h after exercise in TG, but not in WT. Although AMPK and ACC phosphorylation was increased immediately following exercise, the observed exercise-induced autophagy response was not associated with phosphorylation of the AMPK-target ULK1. However, lower protein carbonyl content was observed in lox/lox and TG mice after exercise coinciding with the increased LC3 lipidation. In conclusion, the present results suggest a role of skeletal muscle PGC-1α in coordinating several exercise-induced adaptive responses including autophagic removal of damaged cellular components.

Indexed as

AnimalsAutophagyBlotting, WesternMaleMiceMice, KnockoutMice, TransgenicMuscle, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical Conditioning, AnimalPolymerase Chain ReactionTranscription FactorsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTranscription FactorsAutophagyexercisePGC‐1α

Identifiers

PMID26869683
PMCPMC4758928
OpenAlexW2281774672

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Registered trials

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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.