Late-life rapamycin treatment reverses age-related heart dysfunction

Flynn JM, O'Leary MN, Zambataro CA, Academia EC, Presley MP, Melov S · 2013 · Aging Cell · Atlas ID FLY2013

What this study shows

Striking evidence that in mice mTOR inhibition doesn't just SLOW aging - it can partly reverse an established age-related phenotype. Giving rapamycin to already-old (24-month) mice for 3 months improved aged heart function, reversing age-related cardiac changes via anti-hypertrophic and anti-inflammatory effects. Started late, still worked.

Abstract

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Rapamycin has been shown to extend lifespan in numerous model organisms including mice, with the most dramatic longevity effects reported in females. However, little is known about the functional ramifications of this longevity-enhancing paradigm in mammalian tissues. We treated 24-month-old female C57BL/6J mice with rapamycin for 3 months and determined health outcomes via a variety of noninvasive measures of cardiovascular, skeletal, and metabolic health for individual mice.

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At a glance

Evidence type	A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Aged (24-month) female mice); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Aged (24-month) female mice
Journal	Aging Cell
Year	2013
Peer reviewed	Yes
Record last updated	2026-07-29
Source	DOI 10.1111/acel.12109 · PMID 23734717 · Free full text (PMC4098908)

Extracted findings

Intervention	Rapamycin (3 months, late life)
Target	mTOR
Model	Aged (24-month) female mice
Effect	Late-life rapamycin reverses age-related cardiac dysfunction in aged mice
Dose	oral delivery of microencapsulated rapamycin diet at 14 parts per million (ppm) for 3 months
Sample size	N = 18 for each group (treated vs. nontreated)
Effect size	Significant systemic reduction in 4 cytokines (G-CSF, LIX, IL-17, IL-7) linked to inflammation (n=10 per group, P<0.05)
Limitations	Under- or overestimation of body composition in energy expenditure (EE) calculation is a known pitfall of indirect calorimetry

In the Atlas

Cite this paper

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Flynn, J. M., O'Leary, M. N., Zambataro, C. A., Academia, E. C., Presley, M. P., & Melov, S. (2013). Late-life rapamycin treatment reverses age-related heart dysfunction. Aging Cell. https://doi.org/10.1111/acel.12109

@article{FLY2013,
  author       = {Flynn, J. M. and O'Leary, M. N. and Zambataro, C. A. and Academia, E. C. and Presley, M. P. and Melov, S.},
  title        = {{Late-life rapamycin treatment reverses age-related heart dysfunction}},
  journal      = {Aging Cell},
  year         = {2013},
  doi          = {10.1111/acel.12109},
  note         = {PMID: 23734717},
}

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 FLY2013) [Data set]. https://mtor-atlas.org/study/FLY2013/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_FLY2013,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record FLY2013},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/FLY2013/},
  doi          = {10.5281/zenodo.22059963}
}