Evidence map›Paper›PMID 25375380›Full record

ArticleCell death & disease2014

PGC-1α buffers ROS-mediated removal of mitochondria during myogenesis.

S Baldelli, K Aquilano, M R Ciriolo

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

108 citing papers in PubMed, 168 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mitochondrial stress response and myogenic differentiation.Frontiers in cell and developmental biology · 2024
    Review

48 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

3 authors at 2 institutions in 1 country.

S BaldelliScientific Institute for Research, Hospitalization and Health Care, Università Telematica San Raffaele Roma, Via di Val Cannuta 247, Rome, Italy.
K AquilanoDepartment of Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, Rome, Italy.
M R Ciriolo1] Department of Biology, University of Rome "Tor Vergata", Via della Ricerca Scientifica 1, Rome, Italy [2] IRCCS San Raffaele, Via di Val Cannuta 247, Rome, Italy.
University of Rome Tor Vergata · ITSan Raffaele University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial biogenesis and mitophagy are recognized as critical processes underlying mitochondrial homeostasis. However, the molecular pathway(s) coordinating the balance between these cellular programs is still poorly investigated. Here, we show an induction of the nuclear and mitochondrial peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α) during myogenesis, which in turn co-activates the transcription of nuclear and mtDNA-encoded mitochondrial genes. We demonstrate that PGC-1α also buffers oxidative stress occurring during differentiation by promoting the expression of antioxidant enzymes. Indeed, by downregulating PGC-1α, we observed an impairment of antioxidants expression, which was accompanied by a significant reactive oxygen species (ROS) burst and increase of oxidative damage to proteins. In parallel, we detected a decrease of mitochondrial mass and function as well as increased mitophagy through the ROS/FOXO1 pathway. Upon PGC-1α downregulation, we found ROS-dependent nuclear translocation of FOXO1 and transcription of its downstream targets including mitophagic genes such as LC3 and PINK1. Such events were significantly reverted after treatment with the antioxidant Trolox, suggesting that PGC-1α assures mitochondrial integrity by indirectly buffering ROS. Finally, the lack of PGC-1α gave rise to a decrease in MYOG and a strong induction of atrophy-related ubiquitin ligases FBXO32 (FBXO32), indicative of a degenerative process. Overall, our results reveal that in myotubes, PGC-1α takes center place in mitochondrial homeostasis during differentiation because of its ability to avoid ROS-mediated removal of mitochondria.

Indexed as

AnimalsAntioxidantsCell DifferentiationCell LineChromansForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, DevelopmentalMiceMicrotubule-Associated ProteinsMitochondriaMitochondrial TurnoverMitophagyMuscle CellsMuscle DevelopmentMuscle Proteins6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acidAntioxidantsChromansFbxo32 protein, mouseForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsMuscle ProteinsMyogeninMyog protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseProtein KinasesPTEN-Induced Putative KinaseReactive Oxygen SpeciesSKP Cullin F-Box Protein LigasesTranscription Factors

Identifiers

PMID25375380
PMCPMC4260723
OpenAlexW2036660017

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.