ArticleAging cell2019
Voluntary exercise normalizes the proteomic landscape in muscle and brain and improves the phenotype of progeroid mice.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Quantitative assessment of efficacy and evaluation of feasibility of exercise training protocols in adult and pediatric primary mitochondrial disease.BMC medicine · 2026Pooled it
- Review
- Chrono-Exercise Medicine: Why Biological Timing Matters for Human Health.Biomedicines · 2026Article
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Exercise attenuates the hallmarks of aging: Novel perspectives.Journal of sport and health science · 2025Review
- Hallmarks of aging in age-related macular degeneration and age-related neurological disorders: novel insights into common mechanisms and clinical relevance.Eye (London, England) · 2025Review
- Mitochondrial DNA alterations in precision oncology: Emerging roles in diagnostics and therapeutics.Clinics (Sao Paulo, Brazil) · 2025Review
- Article
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- The impact of COVID-19 on accelerating of immunosenescence and brain aging.Frontiers in cellular neuroscience · 2024Review
- Mechanisms of mechanical overload-induced skeletal muscle hypertrophy: current understanding and future directions.Physiological reviews · 2023Review
- Ageing in the brain: mechanisms and rejuvenating strategies.Cellular and molecular life sciences : CMLS · 2023Review
- SESN1 is a FOXO3 effector that counteracts human skeletal muscle ageing.Cell proliferation · 2023Article
- Mitochondrial and metabolic dysfunction in ageing and age-related diseases.Nature reviews. Endocrinology · 2022Review
- Apoptosis-Inducing Factor Deficiency Induces Tissue-Specific Alterations in Autophagy: Insights from a Preclinical Model of Mitochondrial Disease and Exercise Training Effects.Antioxidants (Basel, Switzerland) · 2022Article
- The mtDNA mutation spectrum in the PolG mutator mouse reveals germline and somatic selection.BMC genomic data · 2021Article
- Progressive alterations in amino acid and lipid metabolism correlate with peripheral neuropathy inScience advances · 2021Article
- Article
- Hallmarks of frailty and osteosarcopenia in prematurely aged PolgAJournal of cachexia, sarcopenia and muscle · 2020Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The accumulation of mitochondrial DNA (mtDNA) mutations is a suspected driver of aging and age-related diseases, but forestalling these changes has been a major challenge. One of the best-studied models is the prematurely aging mtDNA mutator mouse, which carries a homozygous knock-in of a proofreading deficient version of the catalytic subunit of mtDNA polymerase-γ (PolgA). We investigated how voluntary exercise affects the progression of aging phenotypes in this mouse, focusing on mitochondrial and protein homeostasis in both brain and peripheral tissues. Voluntary exercise significantly ameliorated several aspects of the premature aging phenotype, including decreased locomotor activity, alopecia, and kyphosis, but did not have major effects on the decreased lifespan of mtDNA mutator mice. Exercise also decreased the mtDNA mutation load. In-depth tissue proteomics revealed that exercise normalized the levels of about half the proteins, with the majority involved in mitochondrial function and nuclear-mitochondrial crosstalk. There was also a specific increase in the nuclear-encoded proteins needed for the tricarboxylic acid cycle and complex II, but not in mitochondrial-encoded oxidative phosphorylation proteins, as well as normalization of enzymes involved in coenzyme Q biosynthesis. Furthermore, we found tissue-specific alterations, with brain coping better as compared to muscle and with motor cortex being better protected than striatum, in response to mitochondrial dysfunction. We conclude that voluntary exercise counteracts aging in mtDNA mutator mice by counteracting protein dysregulation in muscle and brain, decreasing the mtDNA mutation burden in muscle, and delaying overt aging phenotypes.
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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.