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Mitochondrial DNA Mutations Induce Mitochondrial Dysfunction, Apoptosis and Sarcopenia in Skeletal Muscle of Mitochondrial DNA Mutator Mice

Hiona, Asimina, Sanz, Alberto, Kujoth, Gregory C., Pamplona, Reinald, Seo, Arnold Y., Hofer, Tim, Someya, Shinichi, Miyakawa, Takuya, Nakayama, Chie, Samhan-Arias, Alejandro K., Servais, Stephane, Barger, Jamie L., Portero-Otín, Manuel, Tanokura, Masaru, Prolla, Tomas A., Leeuwenburgh, Christiaan·2010·PLoS ONE

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Crossref · 10.1371/journal.pone.0011468

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  • Cells from mice deficient in mitochondrial DNA polymerase γ show impaired mitochondrial function but this is not accompanied by increased ROS production.

    “Cells from these mice show impaired mitochondrial function but, unexpectedly, this is not accompanied by increased ROS production (Edgar et al., 2009; Hiona et al., 2010).”

    From The Hallmarks of Aging (2013) · cites this paper as Hiona et al., 2010

    The Results (‘Mitochondrial bioenergetics is impaired in D257A mice’; page unavailable) report reduced respiration in skeletal-muscle mitochondria. The Results (‘Skeletal muscle mitochondria from D257A mice produce significantly fewer ROS’; page unavailable) report decreased H2O2 production, supporting the absence of increased ROS. The paper’s measurements are of skeletal-muscle mitochondria, however, not cells from these mice generally. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • In mice, genetic manipulations that impair mitochondrial function but do not increase ROS accelerate aging.

    “genetic manipulations that impair mitochondrial function but do not increase ROS accelerate aging”

    From The Hallmarks of Aging (2013) · cites this paper as Hiona et al., 2010

    The Introduction reports accelerated aging in genetically engineered D257A mice, and the Results report impaired mitochondrial bioenergetics. The Discussion reports decreased mitochondrial ROS production in D257A skeletal muscle, but cautions that ROS production may be tissue-specific. Thus the paper supports the claim for this mouse model, not for genetic manipulations generally or for ROS levels in every tissue. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Dysfunctional mitochondria can contribute to aging independently of ROS, as exemplified by studies with mice deficient in DNA polymerase γ.

    “Dysfunctional mitochondria can contribute to aging independently of ROS, as exemplified by studies with mice deficient in DNA polymerase γ”

    From The Hallmarks of Aging (2013) · cites this paper as Hiona et al., 2010

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Metadata

Authors
Hiona, A., Sanz, A., Kujoth, G. C., Pamplona, R., Seo, A. Y., Hofer, T., Someya, S., Miyakawa, T., Nakayama, C., Samhan-Arias, A. K., Servais, S., Barger, J. L., Portero-Otín, M., Tanokura, M., Prolla, T. A., & Leeuwenburgh, C.
Venue
PLoS ONE
Published
2010-07-07
Volume
5
Issue
7
Pages
e11468
ISSN
1932-6203
Cited by
250
References
11
Language
en

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