Evidence map›Paper›PMID 24296616›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Rapamycin induces pluripotent genes associated with avoidance of replicative senescence.

Tatiana V Pospelova, Tatiana V Bykova, Svetlana G Zubova, Natalia V Katolikova, Natalia M Yartzeva, Valery A Pospelov

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Ligand-specific regulation of a binary enhancer code dictating cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. mTOR Activity and Autophagy in Senescent Cells, a Complex Partnership.International journal of molecular sciences · 2021
    Review
  7. Review
  8. Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020
    Review
  9. Correlative imaging of ionic transport and electronic structure in nano LiChemical communications (Cambridge, England) · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
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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 2 institutions in 1 country.

Tatiana V PospelovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; St.Petersburg State University; St. Petersburg, Russia.
Tatiana V BykovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; St.Petersburg State University; St. Petersburg, Russia.
Svetlana G ZubovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; St.Petersburg State University; St. Petersburg, Russia.
Natalia V KatolikovaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia.
Natalia M YartzevaInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia.
Valery A PospelovInstitute of Cytology; Russian Academy of Sciences; St. Petersburg, Russia; St.Petersburg State University; St. Petersburg, Russia.
Russian Academy of Sciences · RUSt Petersburg University · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary rodent cells undergo replicative senescence, independent from telomere shortening. We have recently shown that treatment with rapamycin during passages 3-7 suppressed replicative senescence in rat embryonic fibroblasts (REFs), which otherwise occurred by 10-14 passages. Here, we further investigated rapamycin-primed cells for an extended number of passages. Rapamycin-primed cells continued to proliferate without accumulation of senescent markers. Importantly, these cells retained the ability to undergo serum starvation- and etoposide-induced cell cycle arrest. The p53/p21 pathway was functional. This indicates that rapamycin did not cause either transformation or loss of cell cycle checkpoints. We found that rapamycin activated transcription of pluripotent genes, oct-4, sox-2, nanog, as well as further upregulated telomerase (tert) gene. The rapamycin-derived cells have mostly non-rearranged, near-normal karyotype. Still, when cultivated for a higher number of passages, these cells acquired a chromosomal marker within the chromosome 3. We conclude that suppression mTORC1 activity may prevent replicative senescence without transformation of rodent cells.

Indexed as

AnimalsAutophagyCell Culture TechniquesCell CycleCell ProliferationCells, CulturedCellular SenescenceFibroblastsHomeodomain ProteinsKaryotypeNanog Homeobox ProteinOctamer Transcription Factor-3RatsSirolimusSOXB1 Transcription FactorsTelomeraseHomeodomain ProteinsNanog Homeobox ProteinNANOG protein, humanOctamer Transcription Factor-3POU5F1 protein, humanSirolimusSOX2 protein, humanSOXB1 Transcription FactorsTelomeraseaginggerosuppressionmTORrapalogssenescence

Identifiers

PMID24296616
PMCPMC3905076
OpenAlexW1976608900

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.