ReviewCurrent opinion in genetics & development2016
Amelioration of premature aging in mtDNA mutator mouse by exercise: the interplay of oxidative stress, PGC-1α, p53, and DNA damage. A hypothesis.
Review in Current opinion in genetics & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 44 citations in OpenAlex.
- The role of exercise-mediated mitochondrial quality control remodeling in aging.Frontiers in cell and developmental biology · 2026Review
- Revisiting the Role of Mitochondrial DNA Mutations in Aging: Bridging Theoretical Expectations with Empirical Observations.Aging and disease · 2025Review
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Exogenous Nucleotides Mitigate Cardiac Aging in SAMP8 Mice by Modulating Energy Metabolism Through AMPK Pathway.Nutrients · 2024Article
- Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species.Frontiers in pharmacology · 2023Review
- Autosomal recessive cerebellar ataxias: a diagnostic classification approach according to ocular features.Frontiers in integrative neuroscience · 2023Article
- Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction.Frontiers in physiology · 2023Review
- The Use of Probiotics Combined with Exercise Affects Thiol/Disulfide Homeostasis, an Oxidative Stress Parameter.Nutrients · 2022Article
- Keeping the beat against time: Mitochondrial fitness in the aging heart.Frontiers in aging · 2022Review
- Red ginseng extract improves skeletal muscle energy metabolism and mitochondrial function in chronic fatigue mice.Frontiers in pharmacology · 2022Article
- The mtDNA mutation spectrum in the PolG mutator mouse reveals germline and somatic selection.BMC genomic data · 2021Article
- Constitutive PGC-1α Overexpression in Skeletal Muscle Does Not Contribute to Exercise-Induced Neurogenesis.Molecular neurobiology · 2021Article
- Mitochondrial DNA mutation exacerbates female reproductive aging via impairment of the NADH/NADAging cell · 2020Article
- The Role of Mitochondria in Vascular Calcification.Journal of translational internal medicine · 2020Review
- Targeting Age-Related Pathways in Heart Failure.Circulation research · 2020Review
- p53: A Key Protein That Regulates Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2020Review
- Article
- Mitochondrial Dysfunction in Aging and Cancer.Journal of clinical medicine · 2019Review
- P53 supports endothelial barrier function via APE1/Ref1 suppression.Immunobiology · 2019Article
- Potential Roles for G-Quadruplexes in Mitochondria.Current medicinal chemistry · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
The mtDNA mutator mouse lacks the proofreading capacity of the sole mtDNA polymerase, leading to accumulation of somatic mtDNA mutations, and a profound premature aging phenotype including elevated oxidative stress and apoptosis, and reduced mitochondrial function. We have previously reported that endurance exercise alleviates the aging phenotype in the mutator mice, reduces oxidative stress, and enhances mitochondrial biogenesis. Here we summarize our findings, with the emphasis on the central role of p53 in these adaptations. We demonstrate that mtDNA in sedentary and exercised PolG mice carry similar amounts of mutations in muscle, but in addition to that sedentary mice have more non-mutational damage, which is mitigated by exercise. It follows therefore that the profound alleviation of the mtDNA mutator phenotype in muscle by exercise may not require a reduction in mtDNA mutational load, but rather a decrease of mtDNA damage and/or oxidative stress. We further hypothesize that the observed 'alleviation without a reduction of mutational load' implies that the oxidative stress in PolG muscle is maintained, at least in part, by the 'malicious cycle', a hypothetical positive feedback potentially driven by the 'transcriptional mutagenesis', that is the conversion of chemically modified nucleotides into mutant RNA bases by the mitochondrial RNA polymerase.
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What OpenQuestion holds
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.