Evidence map›Paper›PMID 21245132›Full record

ArticleThe Journal of biological chemistry2011

Exercise increases mitochondrial PGC-1alpha content and promotes nuclear-mitochondrial cross-talk to coordinate mitochondrial biogenesis.

Adeel Safdar, Jonathan P Little, Andrew J Stokl, Bart P Hettinga, Mahmood Akhtar, Mark A Tarnopolsky

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
15.6field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 301 citations in OpenAlex.

  1. Trial
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  8. Article
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  10. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
    Review
  11. Training-Induced Metabolic Adaptations in Skeletal Muscle.Advances in experimental medicine and biology · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Nutrition research and practice · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. Review

72 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Adeel SafdarDepartment of Kinesiology, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.
Jonathan P Little
Andrew J Stokl
Bart P Hettinga
Mahmood Akhtar
Mark A Tarnopolsky
Pediatrics and Genetics · USMcMaster University · CAInternational College of Applied Kinesiology-USA · US

Funding

CIHR MOP97805
6 · The paper itself

Abstract

Endurance exercise is known to induce metabolic adaptations in skeletal muscle via activation of the transcriptional co-activator peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α). PGC-1α regulates mitochondrial biogenesis via regulating transcription of nuclear-encoded mitochondrial genes. Recently, PGC-1α has been shown to reside in mitochondria; however, the physiological consequences of mitochondrial PGC-1α remain unknown. We sought to delineate if an acute bout of endurance exercise can mediate an increase in mitochondrial PGC-1α content where it may co-activate mitochondrial transcription factor A to promote mtDNA transcription. C57Bl/6J mice (n = 12/group; ♀ = ♂) were randomly assigned to sedentary (SED), forced-endurance (END) exercise (15 m/min for 90 min), or forced endurance +3 h of recovery (END+3h) group. The END group was sacrificed immediately after exercise, whereas the SED and END+3h groups were euthanized 3 h after acute exercise. Acute exercise coordinately increased the mRNA expression of nuclear and mitochondrial DNA-encoded mitochondrial transcripts. Nuclear and mitochondrial abundance of PGC-1α in END and END+3h groups was significantly higher versus SED mice. In mitochondria, PGC-1α is in a complex with mitochondrial transcription factor A at mtDNA D-loop, and this interaction was positively modulated by exercise, similar to the increased binding of PGC-1α at the NRF-1 promoter. We conclude that in response to acute altered energy demands, PGC-1α re-localizes into nuclear and mitochondrial compartments where it functions as a transcriptional co-activator for both nuclear and mitochondrial DNA transcription factors. These results suggest that PGC-1α may dynamically facilitate nuclear-mitochondrial DNA cross-talk to promote net mitochondrial biogenesis.

Indexed as

Physical Conditioning, AnimalAnimalsCell NucleusDNA-Binding ProteinsDNA, MitochondrialEnergy MetabolismFemaleMaleMiceMitochondrial ProteinsMitochondria, MuscleNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical EndurancePromoter Regions, GeneticTrans-ActivatorsDNA-Binding ProteinsDNA, MitochondrialMitochondrial Proteinsmitochondrial transcription factor ANrf1 protein, mouseNuclear Respiratory Factor 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseTrans-ActivatorsTranscription Factors

Identifiers

PMID21245132
PMCPMC3060512
OpenAlexW2049175236

What OpenQuestion holds

Textmetadata
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.