Evidence map›Paper›PMID 22713507›Full record

ArticleAging2012

Mitochondrial fusion by pharmacological manipulation impedes somatic cell reprogramming to pluripotency: new insight into the role of mitophagy in cell stemness.

Alejandro Vazquez-Martin, Sílvia Cufi, Bruna Corominas-Faja, Christina Oliveras-Ferraros, Luciano Vellon, Javier A Menendez

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

83 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Metabolic control of induced pluripotency.Frontiers in cell and developmental biology · 2023
    Review
  12. Review
  13. Article
  14. Review
  15. Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021
    Review
  16. Two Faces of Autophagy in the Struggle against Cancer.International journal of molecular sciences · 2021
    Review
  17. Review
  18. Article
  19. Review
  20. Mitophagy promotes the stemness of bone marrow-derived mesenchymal stem cells.Experimental biology and medicine (Maywood, N.J.) · 2021
    Article

23 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

6 authors at 3 institutions in 1 country.

Alejandro Vazquez-MartinTranslational Research Laboratory, Catalan Institute of Oncology (ICO), Girona, Spain.
Sílvia Cufi
Bruna Corominas-Faja
Christina Oliveras-Ferraros
Luciano Vellon
Javier A Menendez
Catalan Institute for Water Research · ESInstitut Català d'Oncologia · ESInstitut d'Investigació Biomèdica de Girona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have suggested a pivotal role for autophagy in stem cell maintenance and differentiation. Reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) has been also suggested to bio-energetically take advantage of mitochondrial autophagy (mitophagy). We have preliminary addressed how mitophagy might play a role in the regulation of induced pluripotency using mdivi-1 (for mitochondrial division inhibitor), a highly efficacious small molecule that selectively inhibits the self-assembly of DRP1, a member of the dynamin family of large GTPases that mediates mitochondrial fission. At mdivi-1 concentrations that rapidly induced the formation of mitochondrial net-like or collapsed perinuclear mitochondrial structures, we observed that the reprogramming efficiency of mouse embryonic fibroblasts transduced with the Yamanaka three-factor cocktail (OCT4, KLF4, and SOX2) is drastically reduced by more than 95%. Treatment of MEFs with mdivi-1 at the early stages of reprogramming before the appearance of iPSC colonies was sufficient to completely inhibit somatic cell reprogramming. Therefore, the observed effects on reprogramming efficiencies were due likely to the inhibition of the process of reprogramming itself and not to an impairment of iPSC colony survival or growth. Moreover, the typical morphology of established iPSC colonies with positive alkaline phosphatase staining was negatively affected by mdivi-1 exposure. In the presence of mdivi-1, the colony morphology of the iPSCs was lost, and they somewhat resembled fibroblasts. The alkaline phosphatase staining was also significantly reduced, a finding that is indicative of differentiation. Our current findings provide new insight into how mitochondrial division is integrated into the reprogramming factors-driven transcriptional network that specifies the unique pluripotency of stem cells.

Indexed as

AnimalsCell DifferentiationCellular ReprogrammingDynaminsFibroblastsHumansInduced Pluripotent Stem CellsKruppel-Like Factor 4MiceMitochondrial DynamicsMitophagyQuinazolinones3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneDnm1l protein, mouseDynaminsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Quinazolinones

Identifiers

PMID22713507
PMCPMC3409676
OpenAlexW1773217871

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.