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RETRACTED ARTICLE:Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice

Overview of attention for article published in Skeletal Muscle, January 2016
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#17 of 332)
  • High Attention Score compared to outputs of the same age (94th percentile)

Mentioned by

news
1 news outlet
blogs
2 blogs
twitter
15 tweeters
facebook
1 Facebook page

Citations

dimensions_citation
58 Dimensions

Readers on

mendeley
121 Mendeley
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Title
RETRACTED ARTICLE:Exercise-induced mitochondrial p53 repairs mtDNA mutations in mutator mice
Published in
Skeletal Muscle, January 2016
DOI 10.1186/s13395-016-0075-9
Pubmed ID
Authors

Adeel Safdar, Konstantin Khrapko, James M. Flynn, Ayesha Saleem, Michael De Lisio, Adam P. W. Johnston, Yevgenya Kratysberg, Imtiaz A. Samjoo, Yu Kitaoka, Daniel I. Ogborn, Jonathan P. Little, Sandeep Raha, Gianni Parise, Mahmood Akhtar, Bart P. Hettinga, Glenn C. Rowe, Zoltan Arany, Tomas A. Prolla, Mark A. Tarnopolsky

Abstract

Human genetic disorders and transgenic mouse models have shown that mitochondrial DNA (mtDNA) mutations and telomere dysfunction instigate the aging process. Epidemiologically, exercise is associated with greater life expectancy and reduced risk of chronic diseases. While the beneficial effects of exercise are well established, the molecular mechanisms instigating these observations remain unclear. Endurance exercise reduces mtDNA mutation burden, alleviates multisystem pathology, and increases lifespan of the mutator mice, with proofreading deficient mitochondrial polymerase gamma (POLG1). We report evidence for a POLG1-independent mtDNA repair pathway mediated by exercise, a surprising notion as POLG1 is canonically considered to be the sole mtDNA repair enzyme. Here, we show that the tumor suppressor protein p53 translocates to mitochondria and facilitates mtDNA mutation repair and mitochondrial biogenesis in response to endurance exercise. Indeed, in mutator mice with muscle-specific deletion of p53, exercise failed to prevent mtDNA mutations, induce mitochondrial biogenesis, preserve mitochondrial morphology, reverse sarcopenia, or mitigate premature mortality. Our data establish a new role for p53 in exercise-mediated maintenance of the mtDNA genome and present mitochondrially targeted p53 as a novel therapeutic modality for diseases of mitochondrial etiology.

Twitter Demographics

The data shown below were collected from the profiles of 15 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 121 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Brazil 2 2%
Unknown 119 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 25 21%
Student > Master 22 18%
Researcher 14 12%
Student > Doctoral Student 9 7%
Student > Bachelor 9 7%
Other 23 19%
Unknown 19 16%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 35 29%
Agricultural and Biological Sciences 22 18%
Medicine and Dentistry 16 13%
Neuroscience 7 6%
Sports and Recreations 4 3%
Other 8 7%
Unknown 29 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 28. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 April 2021.
All research outputs
#979,857
of 19,479,988 outputs
Outputs from Skeletal Muscle
#17
of 332 outputs
Outputs of similar age
#21,332
of 361,748 outputs
Outputs of similar age from Skeletal Muscle
#1
of 1 outputs
Altmetric has tracked 19,479,988 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 94th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 332 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.0. This one has done particularly well, scoring higher than 95% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 361,748 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 94% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them