ArticleAging cell2020
Exercise training reverses cardiac aging phenotypes associated with heart failure with preserved ejection fraction in male mice.
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 53 papers, 1 of them a synthesis that pooled it.
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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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Exercise and survival benefit in cancer patients: evidence from a comprehensive meta-analysis.GeroScience · 2025Pooled it
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Exercise attenuates the hallmarks of aging: Novel perspectives.Journal of sport and health science · 2025Review
- Expert consensus statement for basic research of animal exercise intervention studies in chronic disease prevention and treatment: A joint position paper of the Exercise Science branch of the Biophysical Society of China and the Metabolism and Genetics branch of the Genetics Society of China.Journal of sport and health science · 2025Article
- Single-Cell Sequencing Identifies the Crucial Role of Mitochondrial Fission-Fusion Imbalance in Heart Failure Progression.Journal of cardiovascular translational research · 2025Article
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- METTL3 Is Essential for Exercise Benefits in Diabetic Cardiomyopathy.Circulation · 2025Article
- Molecular Mediators of the Cardiac Benefits of Exercise.Circulation research · 2025Review
- Article
- Comparative phenotyping of C57BL/6J substrains reveals distinctive patterns of cardiac aging.GeroScience · 2025Article
- Exercise-Induced Cardiac Lymphatic Remodeling Mitigates Inflammation in the Aging Heart.Aging cell · 2025Article
- Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Review
- Review
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- CITED4 gene therapy protects against maladaptive cardiac remodeling after ischemia/reperfusion injury in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Realistic Aspects of Cardiac Ultrasound in Rats: Practical Tips for Improved Examination.Journal of imaging · 2024Review
- Quantification of cardiac capillarization in basement-membrane-immunostained myocardial slices using Segment Anything Model.Scientific reports · 2024Article
- Aging in Heart Failure: Embracing Biology Over Chronology: JACC Family Series.JACC. Heart failure · 2024Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Heart failure with preserved ejection fraction (HFpEF) is the most common type of HF in older adults. Although no pharmacological therapy has yet improved survival in HFpEF, exercise training (ExT) has emerged as the most effective intervention to improving functional outcomes in this age-related disease. The molecular mechanisms by which ExT induces its beneficial effects in HFpEF, however, remain largely unknown. Given the strong association between aging and HFpEF, we hypothesized that ExT might reverse cardiac aging phenotypes that contribute to HFpEF pathophysiology and additionally provide a platform for novel mechanistic and therapeutic discovery. Here, we show that aged (24-30 months) C57BL/6 male mice recapitulate many of the hallmark features of HFpEF, including preserved left ventricular ejection fraction, subclinical systolic dysfunction, diastolic dysfunction, impaired cardiac reserves, exercise intolerance, and pathologic cardiac hypertrophy. Similar to older humans, ExT in old mice improved exercise capacity, diastolic function, and contractile reserves, while reducing pulmonary congestion. Interestingly, RNAseq of explanted hearts showed that ExT did not significantly modulate biological pathways targeted by conventional HF medications. However, it reversed multiple age-related pathways, including the global downregulation of cell cycle pathways seen in aged hearts, which was associated with increased capillary density, but no effects on cardiac mass or fibrosis. Taken together, these data demonstrate that the aged C57BL/6 male mouse is a valuable model for studying the role of aging biology in HFpEF pathophysiology, and provide a molecular framework for how ExT potentially reverses cardiac aging phenotypes in HFpEF.
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Registered trials
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