Rapamycin decelerates cellular senescence

Demidenko ZN, Zubova SG, Bukreeva EI, Pospelov VA, Pospelova TV, Blagosklonny MV · 2009 · Cell Cycle · Atlas ID DEM2009

What this study shows

Blagosklonny's key experiment behind his 'hyperfunction' theory of aging. When a cell's division is blocked but mTOR keeps driving growth, the cell tips into permanent senescence. Rapamycin uncouples the two - keeping arrested cells reversible instead of senescent. Direct evidence that mTOR actively drives the senescent state, not just passively accompanies it.

Abstract

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When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21.

Read the full abstract on PubMed →

At a glance

Evidence type	M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human + rodent cell lines) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is.
Study type	5 - Mechanistic / In Vitro
Model system	Human + rodent cell lines
Journal	Cell Cycle
Year	2009
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.4161/cc.8.12.8606 · PMID 19471117

Extracted findings

These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.

Intervention	Rapamycin (mTOR inhibition)
Target	mTOR
Model	Human + rodent cell lines
Effect	Rapamycin decelerates cellular senescence (geroconversion) during cell-cycle arrest

In the Atlas

Open questions that cite this study

Cited as supporting evidence for the open question How much of rapamycin's healthspan benefit runs through fewer senescent cells?.

Cite this paper

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Demidenko, Z. N., Zubova, S. G., Bukreeva, E. I., Pospelov, V. A., Pospelova, T. V., & Blagosklonny, M. V. (2009). Rapamycin decelerates cellular senescence. Cell Cycle. https://doi.org/10.4161/cc.8.12.8606

@article{DEM2009,
  author       = {Demidenko, Z. N. and Zubova, S. G. and Bukreeva, E. I. and Pospelov, V. A. and Pospelova, T. V. and Blagosklonny, M. V.},
  title        = {{Rapamycin decelerates cellular senescence}},
  journal      = {Cell Cycle},
  year         = {2009},
  doi          = {10.4161/cc.8.12.8606},
  note         = {PMID: 19471117},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record DEM2009) [Data set]. https://mtor-atlas.org/study/DEM2009/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_DEM2009,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record DEM2009},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/DEM2009/},
  doi          = {10.5281/zenodo.22059963}
}

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