ArticleAging cell2020
Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
69 citing papers in PubMed, 100 citations in OpenAlex.
- Established and emerging roles of lysosomal dysfunction in cardiac aging.Nature cardiovascular research · 2026Review
- Short-term mTOR inhibition by rapamycin improves cardiac and endothelial function in older men: a proof-of concept pilot study.GeroScience · 2026Article
- Bench to bedside: is rapamycin headed for the docTOR?GeroScience · 2026Review
- Regulation of survival, growth, and metabolism by neuronal mTOR.GeroScience · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- SIRT1-Mediated Mitochondrial Homeostasis in Cardiac Aging: Molecular Mechanisms and Therapeutic Implications.Aging and disease · 2025Review
- Transcriptional Dysregulation of Autophagy in Aging and Potential Interventions: Insights Into TFEB and FOXOs.Frontiers in bioscience (Landmark edition) · 2025Review
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- Metabolic Regulation of Cardiovascular Aging.Current cardiology reports · 2025Review
- Rapamycin Alleviates Heart Failure Caused by Mitochondrial Dysfunction and SERCA Hypoactivity in Syntaxin 12/13 Deficient Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Roadmap for alleviating the manifestations of ageing in the cardiovascular system.Nature reviews. Cardiology · 2025Review
- Sexual dimorphism in response to intermittent fasting and its impact on the brain.Scientific reports · 2025Article
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- Is Senolytic Therapy in Cardiovascular Diseases Ready for Translation to Clinics?Biomolecules · 2025Review
- Proteostatic Imbalance Drives the Pathogenesis and Age-Related Exacerbation of Heart Failure With Preserved Ejection Fraction.JACC. Basic to translational science · 2025Article
- Article
- The mTOR Signaling Pathway: Key Regulator and Therapeutic Target for Heart Disease.Biomedicines · 2025Review
- Review
- Caloric restriction and its mimetics in heart failure with preserved ejection fraction: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Even in healthy aging, cardiac morbidity and mortality increase with age in both mice and humans. These effects include a decline in diastolic function, left ventricular hypertrophy, metabolic substrate shifts, and alterations in the cardiac proteome. Previous work from our laboratory indicated that short-term (10-week) treatment with rapamycin, an mTORC1 inhibitor, improved measures of these age-related changes. In this report, we demonstrate that the rapamycin-dependent improvement of diastolic function is highly persistent, while decreases in both cardiac hypertrophy and passive stiffness are substantially persistent 8 weeks after cessation of an 8-week treatment of rapamycin in both male and female 22- to 24-month-old C57BL/6NIA mice. The proteomic and metabolomic abundance changes that occur after 8 weeks of rapamycin treatment have varying persistence after 8 further weeks without the drug. However, rapamycin did lead to a persistent increase in abundance of electron transport chain (ETC) complex components, most of which belonged to Complex I. Although ETC protein abundance and Complex I activity were each differentially affected in males and females, the ratio of Complex I activity to Complex I protein abundance was equally and persistently reduced after rapamycin treatment in both sexes. Thus, rapamycin treatment in the aged mice persistently improved diastolic function and myocardial stiffness, persistently altered the cardiac proteome in the absence of persistent metabolic changes, and led to persistent alterations in mitochondrial respiratory chain activity. These observations suggest that an optimal translational regimen for rapamycin therapy that promotes enhancement of healthspan may involve intermittent short-term treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.