A shared mechanism of muscle wasting in cancer and Huntington’s diseaseReport as inadecuate

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Clinical and Translational Medicine

, 4:34

First Online: 14 December 2015Received: 15 October 2015Accepted: 29 November 2015DOI: 10.1186-s40169-015-0076-z

Cite this article as: Mielcarek, M. & Isalan, M. Clin Trans Med 2015 4: 34. doi:10.1186-s40169-015-0076-z


Skeletal muscle loss and dysfunction in aging and chronic diseases is one of the major causes of mortality in patients, and is relevant for a wide variety of diseases such as neurodegeneration and cancer. Muscle loss is accompanied by changes in gene expression and metabolism that lead to contractile impairment and likely affect whole-body metabolism and function. The changes may be caused by inactivity, inflammation, age-related factors or unbalanced nutrition. Although links with skeletal muscle loss have been found in diseases with disparate aetiologies, for example both in Huntington’s disease HD and cancer cachexia, the outcome is a similar impairment and mortality. This short commentary aims to summarize recent achievements in the identification of common mechanisms leading to the skeletal muscle wasting syndrome seen in diseases as different as cancer and HD. The latter is the most common hereditary neurodegenerative disorder and muscle wasting is an important component of its pathology. In addition, possible therapeutic strategies for anti-cachectic treatment will be also discussed in the light of their translation into possible therapeutic approaches for HD.

KeywordsSkeletal muscle atrophy Muscle cachexia Huntington’s disease Neurodegeneration Cancer Energy imbalance AbbreviationsHDHuntington’s disease

TAtibialis anterior

EDLextensor digitorum longus

ACTRIIBactivin receptor type IIB

ALSamyotrophic lateral sclerosis

SMAspinal muscular atrophy

NFκBnuclear factor kappaB

HDAC4histone deacetylase 4

DACH2dachshund homolog 2

Pax7paired box 7

IL-1interleukin 1

p-Stat3phospho-signal transducer and activator of transcription 3

FOXO-3forkhead box O3

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Author: Michal Mielcarek - Mark Isalan

Source: https://link.springer.com/

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