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Comparison of whole body SOD1 knockout with muscle specific SOD1 knockout mice reveals a role for nerve redox signaling in regulation of degenerative pathways in skeletal muscle.

Overview of attention for article published in Antioxidants & Redox Signaling, October 2017
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About this Attention Score

  • Above-average Attention Score compared to outputs of the same age (61st percentile)
  • High Attention Score compared to outputs of the same age and source (81st percentile)

Mentioned by

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4 tweeters

Citations

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18 Dimensions

Readers on

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45 Mendeley
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Title
Comparison of whole body SOD1 knockout with muscle specific SOD1 knockout mice reveals a role for nerve redox signaling in regulation of degenerative pathways in skeletal muscle.
Published in
Antioxidants & Redox Signaling, October 2017
DOI 10.1089/ars.2017.7249
Pubmed ID
Authors

Sakellariou, Giorgos, McDonagh, Brian, Porter, Helen, Giakoumaki, Ifigeneia, Earl, Kate, Nye, Gareth, Vasilaki, Aphrodite, Brooks, Susan, Richardson, Arlan, Van Remmen, Holly, McArdle, Anne, Jackson, Malcolm Joseph, SakellariouGiorgos K., McDonaghBrian, PorterHelen, GiakoumakiIfigeneia I., EarlKate E., NyeGareth A., VasilakiAphrodite, BrooksSusan V., RichardsonArlan, Van RemmenHolly, McArdleAnne, JacksonMalcolm J., Giorgos K. Sakellariou, Brian McDonagh, Helen Porter, Ifigeneia I. Giakoumaki, Kate E. Earl, Gareth A. Nye, Aphrodite Vasilaki, Susan V. Brooks, Arlan Richardson, Holly Van Remmen, Anne McArdle, Malcolm J. Jackson

Abstract

Lack of CuZnSOD in homozygous knockout mice (Sod1-/-) leads to accelerated age-related muscle loss and weakness, but specific deletion of CuZnSOD in skeletal muscle(mSod1KO mice) or neurons (nSod1KO mice) resulted in only mild muscle functional deficits and failed to recapitulate the loss of mass and function observed in Sod1-/- mice. To dissect any underlying cross-talk between motor neurons and skeletal muscle in the degeneration in Sod1-/- mice, we characterized neuromuscular changes in the Sod1-/- model compared with mSod1KO mice and examined degenerative molecular mechanisms and pathways in peripheral nerve and skeletal muscle. In contrast to mSod1KO mice, myofiber atrophy in Sod1-/- mice was associated with increased muscle oxidative damage, neuromuscular junction degeneration, denervation, nerve demyelination and upregulation of proteins involved in maintenance of myelin sheaths. Proteomic analyses confirmed increased proteasomal activity and adaptive stress responses in muscle of Sod1-/- mice that were absent in mSod1KO mice. Peripheral nerve from neither Sod1-/- nor mSod1KO mice showed increased oxidative damage or molecular responses to increased oxidation compared with wild type mice. Differential Cysteine labelling revealed a specific redox shift in the catalytic Cysteine residue of peroxiredoxin 6 (Cys47) in the peripheral nerve from Sod1-/- mice. Innovation and Conclusion: These findings demonstrate that neuromuscular integrity, redox mechanisms and pathways are differentially altered in nerve and muscle of Sod1-/- and mSod1KO mice. Results support the concept that impaired redox signaling, rather than oxidative damage, in peripheral nerve plays a key role in muscle loss in Sod1-/- mice and potentially sarcopenia during aging.

Twitter Demographics

The data shown below were collected from the profiles of 4 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 45 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 45 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 18%
Student > Doctoral Student 6 13%
Student > Master 5 11%
Researcher 5 11%
Student > Bachelor 5 11%
Other 11 24%
Unknown 5 11%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 18 40%
Agricultural and Biological Sciences 6 13%
Medicine and Dentistry 6 13%
Neuroscience 5 11%
Arts and Humanities 1 2%
Other 2 4%
Unknown 7 16%

Attention Score in Context

This research output has an Altmetric Attention Score of 3. 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 01 September 2018.
All research outputs
#6,838,563
of 13,454,271 outputs
Outputs from Antioxidants & Redox Signaling
#527
of 1,230 outputs
Outputs of similar age
#118,966
of 312,401 outputs
Outputs of similar age from Antioxidants & Redox Signaling
#4
of 22 outputs
Altmetric has tracked 13,454,271 research outputs across all sources so far. This one is in the 48th percentile – i.e., 48% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,230 research outputs from this source. They receive a mean Attention Score of 4.0. This one has gotten more attention than average, scoring higher than 56% 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 312,401 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 61% of its contemporaries.
We're also able to compare this research output to 22 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 81% of its contemporaries.