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Role of telomere dysfunction in cardiac failure in Duchenne muscular dystrophy

Overview of attention for article published in Nature Cell Biology, July 2013
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (97th percentile)
  • High Attention Score compared to outputs of the same age and source (91st percentile)

Mentioned by

news
5 news outlets
blogs
1 blog
twitter
10 tweeters
facebook
1 Facebook page
wikipedia
1 Wikipedia page
googleplus
1 Google+ user

Citations

dimensions_citation
73 Dimensions

Readers on

mendeley
136 Mendeley
Title
Role of telomere dysfunction in cardiac failure in Duchenne muscular dystrophy
Published in
Nature Cell Biology, July 2013
DOI 10.1038/ncb2790
Pubmed ID
Authors

Foteini Mourkioti, Jackie Kustan, Peggy Kraft, John W. Day, Ming-Ming Zhao, Maria Kost-Alimova, Alexei Protopopov, Ronald A. DePinho, Daniel Bernstein, Alan K. Meeker, Helen M. Blau

Abstract

Duchenne muscular dystrophy (DMD), the most common inherited muscular dystrophy of childhood, leads to death due to cardiorespiratory failure. Paradoxically, mdx mice with the same genetic deficiency of dystrophin exhibit minimal cardiac dysfunction, impeding the development of therapies. We postulated that the difference between mdx and DMD might result from differences in telomere lengths in mice and humans. We show here that, like DMD patients, mice that lack dystrophin and have shortened telomeres (mdx/mTR(KO)) develop severe functional cardiac deficits including ventricular dilation, contractile and conductance dysfunction, and accelerated mortality. These cardiac defects are accompanied by telomere erosion, mitochondrial fragmentation and increased oxidative stress. Treatment with antioxidants significantly retards the onset of cardiac dysfunction and death of mdx/mTR(KO) mice. In corroboration, all four of the DMD patients analysed had 45% shorter telomeres in their cardiomyocytes relative to age- and sex-matched controls. We propose that the demands of contraction in the absence of dystrophin coupled with increased oxidative stress conspire to accelerate telomere erosion culminating in cardiac failure and death. These findings provide strong support for a link between telomere length and dystrophin deficiency in the etiology of dilated cardiomyopathy in DMD and suggest preventive interventions.

Twitter Demographics

The data shown below were collected from the profiles of 10 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 136 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 2 1%
Spain 1 <1%
United States 1 <1%
Argentina 1 <1%
Unknown 131 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 32 24%
Student > Bachelor 31 23%
Researcher 28 21%
Student > Master 13 10%
Student > Doctoral Student 8 6%
Other 24 18%
Readers by discipline Count As %
Agricultural and Biological Sciences 75 55%
Biochemistry, Genetics and Molecular Biology 19 14%
Medicine and Dentistry 18 13%
Unspecified 9 7%
Neuroscience 4 3%
Other 11 8%

Attention Score in Context

This research output has an Altmetric Attention Score of 56. 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 15 May 2014.
All research outputs
#311,232
of 13,517,557 outputs
Outputs from Nature Cell Biology
#198
of 3,117 outputs
Outputs of similar age
#3,752
of 153,357 outputs
Outputs of similar age from Nature Cell Biology
#6
of 70 outputs
Altmetric has tracked 13,517,557 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 97th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 3,117 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 15.3. This one has done particularly well, scoring higher than 93% 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 153,357 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 97% of its contemporaries.
We're also able to compare this research output to 70 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 91% of its contemporaries.