RETRACTED: Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice
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Post-publication record
- Nature
- Retraction
- Reason
- Author Unresponsive;Concerns/Issues about Image;Duplication of/in Image;Investigation by Company/Institution;Investigation by Third Party;Upgrade/Update of Prior Notice(s);
- Date
- 10/6/2025 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
A causal role for mitochondrial DNA (mtDNA) mutagenesis in mammalian aging is supported by recent studies demonstrating that the mtDNA mutator mouse, harboring a defect in the proofreading-exonuclease activity of mitochondrial polymerase gamma, exhibits accelerated aging phenotypes characteristic of human aging, systemic mitochondrial dysfunction, multisystem pathology, and reduced lifespan. Epidemiologic studies in humans have demonstrated that endurance training reduces the risk of chronic diseases and extends life expectancy. Whether endurance exercise can attenuate the cumulative systemic decline observed in aging remains elusive. Here we show that 5 mo of endurance exercise induced systemic mitochondrial biogenesis, prevented mtDNA depletion and mutations, increased mitochondrial oxidative capacity and respiratory chain assembly, restored mitochondrial morphology, and blunted pathological levels of apoptosis in multiple tissues of mtDNA mutator mice. These adaptations conferred complete phenotypic protection, reduced multisystem pathology, and prevented premature mortality in these mice. The systemic mitochondrial rejuvenation through endurance exercise promises to be an effective therapeutic approach to mitigating mitochondrial dysfunction in aging and related comorbidities.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
The record
- Venue
- Proceedings of the National Academy of Sciences
- Topic
- Mitochondrial Function and Pathology
- Field
- Biochemistry, Genetics and Molecular Biology
- Canadian institutions
- McMaster University
- Funders
- National Institute on AgingCanadian Institutes of Health Research
- Keywords
- Mitochondrial DNAMitochondrial biogenesisPremature agingBiologyWerner syndromeMitochondrionGeneticsTFAMEndurance trainingHeteroplasmyPhenotypeRejuvenationProteostasisOxidative stressCell biologyEndocrinologyGene
- Has abstract in OpenAlex
- yes