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Skeletal muscle atrophy: disease-induced mechanisms may mask disuse atrophy

Overview of attention for article published in Journal of Muscle Research and Cell Motility, January 2016
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About this Attention Score

  • Among the highest-scoring outputs from this source (#27 of 188)
  • Good Attention Score compared to outputs of the same age (67th percentile)
  • Good Attention Score compared to outputs of the same age and source (66th percentile)

Mentioned by

twitter
5 tweeters
facebook
1 Facebook page

Citations

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18 Dimensions

Readers on

mendeley
61 Mendeley
Title
Skeletal muscle atrophy: disease-induced mechanisms may mask disuse atrophy
Published in
Journal of Muscle Research and Cell Motility, January 2016
DOI 10.1007/s10974-015-9439-8
Pubmed ID
Authors

C. J. Malavaki, G. K. Sakkas, G. I. Mitrou, A. Kalyva, I. Stefanidis, K. H. Myburgh, C. Karatzaferi

Abstract

Disuse atrophy is the loss of skeletal muscle mass due to inactivity or lower than 'normal' use. It is not only a furtive component of the 'modern' sedentary lifestyle but also a part of numerous pathologies, where muscle loss is linked to disease specific and/or other toxicity factors, eventually leading to wasting (cachexia). Whether disuse-or-disease induced, muscle loss leads to weakness and metabolic comorbidities with a high societal and financial cost. This review discusses the intricate network of interacting signalling pathways including Atrogin-1/MAFbx, IGF1-Akt, myostatin, glucocorticoids, NF-kB, MAPKs and caspases that seem to regulate disuse atrophy but also share common activation patterns in other states of muscle loss such as sarcopenia or cachexia. Reactive oxygen species are also important regulators of cell signalling pathways that can accelerate proteolysis and depress protein synthesis. Exercise is an effective countermeasure and antioxidants may show some benefit. We discuss how the experimental model used can crucially affect the outcome and hence our understanding of atrophy. Timing of sampling is crucial as some signalling mechanisms reach their peak early during the atrophy process to rapidly decline thereafter, while other present high levels even weeks and months after study initiation. The importance of such differences lays in future consideration of appropriate treatment targets. Apart from attempting to correct defective genes or negate their effects, technological advances in new rational ways should aim to regulate specific gene expression at precise time points for the treatment of muscle atrophy in therapeutic protocols depending on the origin of atrophy induction.

Twitter Demographics

The data shown below were collected from the profiles of 5 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 61 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 2%
Unknown 60 98%

Demographic breakdown

Readers by professional status Count As %
Student > Master 12 20%
Unspecified 10 16%
Student > Ph. D. Student 9 15%
Student > Bachelor 8 13%
Student > Postgraduate 5 8%
Other 17 28%
Readers by discipline Count As %
Unspecified 14 23%
Medicine and Dentistry 10 16%
Biochemistry, Genetics and Molecular Biology 9 15%
Nursing and Health Professions 9 15%
Agricultural and Biological Sciences 7 11%
Other 12 20%

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 08 January 2016.
All research outputs
#3,547,608
of 12,343,108 outputs
Outputs from Journal of Muscle Research and Cell Motility
#27
of 188 outputs
Outputs of similar age
#100,260
of 337,551 outputs
Outputs of similar age from Journal of Muscle Research and Cell Motility
#2
of 9 outputs
Altmetric has tracked 12,343,108 research outputs across all sources so far. This one is in the 49th percentile – i.e., 49% of other outputs scored the same or lower than it.
So far Altmetric has tracked 188 research outputs from this source. They receive a mean Attention Score of 2.7. This one is in the 36th percentile – i.e., 36% of its peers scored the same or lower than it.
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 337,551 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 67% of its contemporaries.
We're also able to compare this research output to 9 others from the same source and published within six weeks on either side of this one. This one has scored higher than 7 of them.