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

  • Marina Bouchè | marina.bouche@uniroma1.it DAHFMO, Unit of Histology, Sapienza University of Rome; Interuniversity Institute of Myology, Italy.
  • Biliana Lozanoska-Ochser DAHFMO, Unit of Histology, Sapienza University of Rome, Rome, Italy.
  • Daisy Proietti DAHFMO, Unit of Histology, Sapienza University of Rome; IRCCS, Fondazione Santa Lucia, Rome, Italy.
  • Luca Madaro IRCCS, Fondazione Santa Lucia, Rome; Interuniversity Institute of Myology, Italy.

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.

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Author Biography

Marina Bouchè, DAHFMO, Unit of Histology, Sapienza University of Rome; Interuniversity Institute of Myology

DAHFMO, Unit of Histology

Published
2018-12-13
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Section
Perspectives
Supporting Agencies
Sapienza University of Rome, Parent Project Onlus Italy, Dutch Parent Project, Italian Ministry of Health
Keywords:
muscle atrophy, cancer cachexia, neurogenic muscle atrophy, ubiquitin-proteasome, autophagy
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How to Cite
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). https://doi.org/10.4081/ejtm.2018.7931