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Lookup NU author(s): Dr Elizabeth Stoll, Nevena Karapavlovic, Hannah Rosa, Michael Woodmass, Dr Karolina Rygiel, Dr Kathryn White, Emeritus Professor Doug Turnbull
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
The naked mole-rat (NMR) Heterocephalus glaber is an exceptionally long-lived rodent, living up to 32 years in captivity. This extended lifespan is accompanied by a phenotype of negligible senescence, a phenomenon of very slow changes in the expected physiological characteristics with age. One of the many consequences of normal aging in mammals is the devastating and progressive loss of skeletal muscle, termed sarcopenia, caused in part by respiratory enzyme dysfunction within the mitochondria of skeletal muscle fibers. Here we report that NMRs avoid sarcopenia for decades. Muscle fiber integrity and mitochondrial ultrastructure are largely maintained in aged animals. While mitochondrial Complex IV expression and activity remains stable, Complex I expression is significantly decreased. We show that aged naked mole-rat skeletal muscle tissue contains some mitochondrial DNA rearrangements, although the common mitochondrial DNA deletions associated with aging in human and other rodent skeletal muscles are not present. Interestingly, NMR skeletal muscle fibers demonstrate a significant increase in mitochondrial DNA copy number. These results have intriguing implications for the role of mitochondria in aging, suggesting Complex IV, but not Complex I, function is maintained in the long-lived naked mole rat, where sarcopenia is avoided and healthy muscle function is maintained for decades.
Author(s): Stoll EA, Karapavlovic N, Rosa H, Woodmass M, Rygiel K, White K, Turnbull DM, Faulkes CG
Publication type: Article
Publication status: Published
Journal: Aging (Albany)
Year: 2016
Volume: 8
Issue: 12
Pages: 3468–3483
Online publication date: 19/12/2016
Acceptance date: 05/12/2016
Date deposited: 05/02/2017
ISSN (electronic): 1945-4589
Publisher: Impact Journals LLC
URL: http://dx.doi.org/10.18632/aging.101140
DOI: 10.18632/aging.101140
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