Late-life rapamycin treatment reverses age-related heart dysfunction
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) female mice for 3 months improved aged heart function, reversing or attenuating age-related cardiac changes, with RNA-seq changes suggesting anti-hypertrophic and anti-inflammatory effects. Started late, still worked.
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
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 (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
Related topics
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