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

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.

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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}
}