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Bouchè M, Lozanoska-Ochser B, Proietti D, et al. Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?. Eur J Transl Myol. 2018;28(4):7931doi: 10.4081/ejtm.2018.7931.
Bouchè, M., Lozanoska-Ochser, B., Proietti, D., & Madaro, L. (2018). Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?. European journal of translational myology, 28(4), 7931. https://doi.org/10.4081/ejtm.2018.7931
Bouchè, Marina, et al. "Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?." European journal of translational myology vol. 28,4 (2018): 7931. doi: https://doi.org/10.4081/ejtm.2018.7931
Bouchè M, Lozanoska-Ochser B, Proietti D, Madaro L. Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?. Eur J Transl Myol. 2018 Dec 13;28(4):7931. doi: 10.4081/ejtm.2018.7931. eCollection 2018 Nov 02. PMID: 30662704; PMCID: PMC6317130.
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Eur J Transl Myol. 2018 Dec 13;28(4):7931. doi: 10.4081/ejtm.2018.7931. eCollection 2018 Nov 02.

Do neurogenic and cancer-induced muscle atrophy follow common or divergent paths?.

European journal of translational myology

Marina Bouchè, Biliana Lozanoska-Ochser, Daisy Proietti, Luca Madaro

Affiliations

  1. DAHFMO, Unit of Histology, Sapienza University of Rome, 00161 Rome, Italy.
  2. Interuniversity Institute of Myology, Italy.
  3. IRCCS, Fondazione Santa Lucia, Rome, Italy.

PMID: 30662704 PMCID: PMC6317130 DOI: 10.4081/ejtm.2018.7931

Abstract

Skeletal muscle is a dynamic tissue capable of responding to a large variety of physiological stimuli by adjusting muscle fiber size, metabolism and function. However, in pathological conditions such as cancer and neural disorders, this finely regulated homeostasis is impaired leading to severe muscle wasting, reduced muscle fiber size (atrophy), and impaired function. These disease features develop due to enhanced protein breakdown, which relies on two major degradation systems: the ubiquitin-proteasome and the autophagy-lysosome. These systems are independently regulated by different signalling pathways, which in physiological conditions, determine protein and organelle turnover. However, alterations in one or both systems, as it happens in several disorders, leads to enhanced protein breakdown and muscle atrophy. Although this is a common feature in the different types of muscle atrophy, the relative contribution of each of these systems is still under debate. Here, we will briefly describe the regulation and the activity of the ubiquitin-proteasome and the autophagy-lysosome systems during muscle wasting. We will then discuss what we know regarding how these pathways are involved in cancer induced and in neurogenic muscle atrophy, highlighting common and divergent paths. It is now clear that there is no one unifying common mechanism that can be applied to all models of muscle loss. Detailed understanding of the pathways and proteolysis mechanisms involved in each model will hopefully help the development of drugs to counteract muscle wasting in specific conditions.

Keywords: autophagy; cancer cachexia; muscle atrophy; neurogenic muscle atrophy; ubiquitin-proteasome

Conflict of interest statement

Conflict of Interest None of the authors have conflicts of interests.

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