Oliver's mTOR Atlas Evidence Platform
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Cardiac aging

Outcome · 4 studies in the Atlas

Age-related decline in heart function (hypertrophy, stiffening, reduced contractility). Late-life rapamycin partially reversed it in aged female mice (FLY2013); male mice were not tested.

The gradual decline in heart function with age - thicker heart muscle, stiffer walls, weaker pumping. In old female mice, giving rapamycin late in life partly reversed these changes; male mice were not tested.

Age-related decline in heart function (hypertrophy, stiffening, reduced contractility). Late-life rapamycin partially reversed it in aged female mice (FLY2013); male mice were not tested.

TL;DR. Cardiac aging appears in 4 curated studies in Oliver's mTOR Atlas: 4 in animal models. No study in people is recorded for it in the Atlas yet.

Evidence at a glance

EvidenceWhat it meansStudies
A Animal model4

No direct human evidence in the Atlas for this entity yet — everything below rests on animal or molecular work.

Studies

YearEvidenceStudy
2026 A Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation. JIN2026B Dietary rapamycin reduced aging-induced atrial fibrillation susceptibility and atrial remodelling in D-galactose-aged mice, acting through mTOR-independent inhibition of HIF-1α plus restored mitochondrial function and insulin sensitivity.
2023 A A masked, placebo-controlled, randomized clinical trial evaluating safety and the effect on cardiac function of low-dose rapamycin in 17 healthy client-owned dogs BAR2023 In 17 healthy pet dogs, 6 months of low-dose rapamycin (0.025 mg/kg, three times a week) caused no clinically significant adverse events. Echocardiography, however, showed NO statistically significant difference from placebo at 6 or 12 months, so the heart benefit hinted at in the earlier 10-week trial (URF2017) was not reproduced. Owners did report perceived positive changes in behavior or health more often in the rapamycin group (26.8% vs 8.1% of bi-weekly surveys), but that is a subjective, owner-reported outcome. A small safety-focused trial, not designed to test lifespan.
2016 A Cardioprotection and lifespan extension by the natural polyamine spermidine EIS2016 The mammalian follow-up to EIS2009 and the reason the spermidine branch matters for human health claims: oral spermidine extends mouse lifespan, reduces cardiac hypertrophy and preserves diastolic function, and the protection disappears in mice whose cardiomyocytes lack Atg5, which makes autophagy necessary rather than merely correlated. Boundary: the human part is a dietary questionnaire correlated with blood pressure and cardiovascular incidence, so it is observational and does not carry the causal claim the mouse data carry.
2013 A Late-life rapamycin treatment reverses age-related heart dysfunction FLY2013 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.

Related entities

Longevity 3Rapamycin 3mTOR 2HIF-1α 1Atg5 1SpermidineAtrial fibrillationmTORC1 1Autophagy 1

Cite this page

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Barton, O. (2026). Cardiac aging [Entity page]. In Oliver's mTOR Atlas [Data set]. https://mtor-atlas.org/outcome/cardiac-aging/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_outcome_cardiac_aging,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}: Cardiac aging},
  howpublished = {Entity page in a data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/outcome/cardiac-aging/},
  doi          = {10.5281/zenodo.22059963}
}
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