Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition

Blagosklonny MV · 2006 · Cell Cycle · Atlas ID BLA2006

What this study shows

Proposes the 'hyperfunction theory' of aging: TOR signaling, useful in youth, stays switched on into old age and becomes actively damaging.

Abstract

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While ruling out programmed aging, evolutionary theory predicts a quasi-program for aging, a continuation of the developmental program that is not turned off, is constantly on, becoming hyper-functional and damaging, causing diseases of aging. Could it be switched off pharmacologically? This would require identification of a molecular target involved in cell senescence, organism aging and diseases of aging. Notably, cell senescence is associated with activation of the TOR (target of rapamycin) nutrient- and mitogen-sensing pathway, which promotes cell growth, even though cell cycle is blocked.

Read the full abstract on PubMed →

At a glance

Evidence type	R Review — secondary literature, not a new result Marked R because it is a review or synthesis of existing evidence rather than a new primary result; that is a different form of writing, not a weaker one.
Study type	Narrative Review
Model system	Theoretical / review article
Journal	Cell Cycle
Year	2006
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.4161/cc.5.18.3288 · PMID 17012837

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	Not applicable (theoretical/review; proposes rapamycin)
Target	mTOR
Model	Theoretical / review article
Effect	Proposes aging as a quasi-programmed, hyperfunctional mTOR-driven process that rapamycin could pharmacologically slow

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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Blagosklonny, M. V. (2006). Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition. Cell Cycle. https://doi.org/10.4161/cc.5.18.3288

@article{BLA2006,
  author       = {Blagosklonny, M. V.},
  title        = {{Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition}},
  journal      = {Cell Cycle},
  year         = {2006},
  doi          = {10.4161/cc.5.18.3288},
  note         = {PMID: 17012837},
}

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 BLA2006) [Data set]. https://mtor-atlas.org/study/BLA2006/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_BLA2006,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record BLA2006},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/BLA2006/},
  doi          = {10.5281/zenodo.22059963}
}

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