Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation.

Jin L, Jiang T, Gong H, Gong L, Wang Y, Chen Z, Liu P, Qin X, Zheng Q · 2026 · Biochimica et Biophysica Acta - Molecular Basis of Disease · Atlas ID JIN2026B

What this study shows

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.

Abstract

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Atrial fibrillation (AF) is an age-related disease. Although rapamycin is a foremost anti-aging therapy with proven efficacy in lifespan extension, its impact on aging-induced atrial remodeling and AF susceptibility was unknown. An aging-induced AF-susceptible mouse model was produced by D-galactose injection followed by a rapamycin diet. Rapamycin significantly reduced aging-induced AF susceptibility and ameliorated atrial electrical and structural remodeling.

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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: Mouse (D-galactose aging model)); the code names the system studied -- animal work can be rigorous and still not be human data.
Study type	4 - Animal Study
Model system	Mouse (D-galactose aging model)
Journal	Biochimica et Biophysica Acta - Molecular Basis of Disease
Year	2026
Peer reviewed	Yes
Record last updated	2026-10-01
Source	DOI 10.1016/j.bbadis.2026.168438 · PMID 42648451

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 (dietary)
Target	HIF-1α (mTOR-independent); mitochondrial metabolism
Model	Mouse
Effect	Reduced AF susceptibility, improved insulin resistance, restored mitochondrial function and substrate utilisation

In the Atlas

Cite this paper

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Jin, L., Jiang, T., Gong, H., Gong, L., Wang, Y., Chen, Z., Liu, P., Qin, X., & Zheng, Q. (2026). Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation. Biochimica et Biophysica Acta - Molecular Basis of Disease. https://doi.org/10.1016/j.bbadis.2026.168438

@article{JIN2026B,
  author       = {Jin, L. and Jiang, T. and Gong, H. and Gong, L. and Wang, Y. and Chen, Z. and Liu, P. and Qin, X. and Zheng, Q.},
  title        = {{Rapamycin attenuates age-related atrial remodeling and fibrillation by targeting HIF-1α-mediated metabolic dysregulation}},
  journal      = {Biochimica et Biophysica Acta - Molecular Basis of Disease},
  year         = {2026},
  doi          = {10.1016/j.bbadis.2026.168438},
  note         = {PMID: 42648451},
}

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 JIN2026B) [Data set]. https://mtor-atlas.org/study/JIN2026B/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_JIN2026B,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record JIN2026B},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/JIN2026B/},
  doi          = {10.5281/zenodo.22059963}
}

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