Cited by 320

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

RETRACTED: Endurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice

Safdar, Adeel, Bourgeois, Jacqueline M., Ogborn, Daniel I., Little, Jonathan P., Hettinga, Bart P., Akhtar, Mahmood, Thompson, James E., Melov, Simon, Mocellin, Nicholas J., Kujoth, Gregory C., Prolla, Tomas A., Tarnopolsky, Mark A.·2011·Proceedings of the National Academy of Sciences

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.

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Crossref · 10.1073/pnas.1019581108This paper is marked retracted.

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  • Endurance training and alternate-day-fasting may improve healthspan through their capacity to avoid mitochondrial degeneration.

    “endurance training and alternate-day-fasting may improve healthspan through their capacity to avoid mitochondrial degeneration”

    From The Hallmarks of Aging (2013) · cites this paper as Safdar et al., 2011

    The Abstract reports that endurance exercise prevented mitochondrial dysfunction and premature-aging effects in mtDNA mutator mice, supporting the endurance-training part of the claim. The paper does not report a comparable finding for alternate-day fasting (searched: “alternate-day fasting” and “fasting caloric restriction intermittent alternate day”). (LLM, conf=0.88)

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Metadata

Authors
Safdar, A., Bourgeois, J. M., Ogborn, D. I., Little, J. P., Hettinga, B. P., Akhtar, M., Thompson, J. E., Melov, S., Mocellin, N. J., Kujoth, G. C., Prolla, T. A., & Tarnopolsky, M. A.
Affiliations
  • Departments of aKinesiology,
  • Pathology and Molecular Medicine, and
  • McMaster University
  • Pediatrics,
  • Roswell Park Cancer Institute
  • Buck Institute for Age Research
  • University of Wisconsin
Venue
Proceedings of the National Academy of Sciences
Published
2011-02-22
Volume
108
Issue
10
Pages
4135-4140
ISSN
  • 0027-8424
  • 1091-6490
Cited by
320
References
8
Language
en
Status
Retracted

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