Rapamycin in aged mice: less atrial fibrillation and remodeling via HIF-1α
In a D-galactose-induced aging mouse model, a rapamycin diet reduced atrial fibrillation susceptibility and atrial electrical and structural remodeling; the abstract attributes this mainly to inhibition of HIF-1α and improved downstream metabolism. [1]
Automatic summary · not editorially reviewed
The key findings
Mice made susceptible to atrial fibrillation by D-galactose injection were then given a rapamycin diet. [1]
Rapamycin significantly reduced aging-induced atrial fibrillation susceptibility and ameliorated atrial electrical and structural remodeling. [1]
Restoring mTOR activity did not reverse rapamycin-mediated HIF-1α inhibition, suggesting an mTOR-independent mechanism. [1]
The source at a glance
- Study type / format
- Preclinical animal and cell study (abstract)
- Population / context
- Mice in a D-galactose-induced aging model, plus cell experiments
- Summary based on
- Study abstract
- Original publication
- August 26, 2026
Aged mouse model given rapamycin diet
The abstract describes mice made susceptible to atrial fibrillation by D-galactose injection, an aging-inducing model, and then given a rapamycin diet. The stated aim was to test rapamycin against aging-related atrial fibrillation and to clarify mechanisms. Outcomes examined were atrial fibrillation susceptibility, atrial electrical and structural remodeling, and mechanistic analyses. This is preclinical work in mice; the abstract reports no human participants or human outcomes.
Supporting source [1]
Less atrial fibrillation and remodeling in treated mice
According to the abstract, rapamycin significantly reduced aging-induced atrial fibrillation susceptibility and ameliorated atrial electrical and structural remodeling. Metabolically, it improved systemic insulin resistance, restored mitochondrial function and morphology, and counteracted aging-induced changes in substrate utilization. Mechanistically, rapamycin inhibited HIF-1α transcriptional activity. Cell experiments confirmed direct suppression of CoCl₂-induced HIF-1α expression and nuclear translocation, and restoring HIF-1α attenuated rapamycin's protection against D-galactose-induced atrial structural remodeling.
Supporting source [1]
Suggested direct HIF-1α interaction, mTOR-independent
The abstract reports that molecular docking, dynamics simulations and isothermal titration calorimetry suggested rapamycin may also directly interfere with HIF-1α dimerization. Restoration of mTOR activity did not reverse rapamycin-mediated HIF-1α inhibition, suggesting an mTOR-independent regulatory mechanism. The authors conclude that rapamycin mitigates aging-induced atrial remodeling and atrial fibrillation susceptibility in mice, primarily through HIF-1α inhibition and improved downstream metabolic dysregulation. These are mouse and cell findings; the abstract does not show that rapamycin prevents atrial fibrillation or extends lifespan in humans.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from a D-galactose-induced mouse model and cell experiments, not from human studies. The abstract reports no sample sizes, follow-up duration or effect estimates, and the docking and simulation results are described as suggestions.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Jin L, Jiang T, Gong H, Gong L, Wang Y, Chen Z, Liu P, Qin X, Zheng Q. · europepmc.org · August 26, 2026