Special Issue "Skeletal Muscle Atrophy: Mechanisms at a Cellular Level"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 October 2020.

Special Issue Editors

Dr. Maria Pennuto
Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Italy
Interests: neurodegenerative diseases; androgens; polyglutamine; metabolism; skeletal muscle
Dr. Marco Pirazzini
Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Italy
Interests: neurotoxins; muscle paralysis; neuromuscular junction; neuromuscular disorders; nerve regeneration

Special Issue Information

Dear Colleagues,

Skeletal muscles constitute the largest body organ, making up about half of a mammal’s bodyweight. Several conditions, including neuromuscular disorders, aging, cancer, and those associated with toxins, can lead to losses in muscle mass and function. This acquired condition, referred to as muscle atrophy, is an emerging health concern and a burden for human health. The cellular and molecular factors involved in muscle atrophy are still relatively unknown, despite great effort being made over the last two decades to decipher the pathophysiological bases underlying muscle loss. A wide range of cellular (e.g., myocites and satellite cells) and subcellular (e.g., neuromuscular junctions) compartments, organelles (e.g., mitochondria, ER, SR), degradation pathways (e.g., UPS and autophagy), molecular signaling networks (e.g., AKT, mTOR, etc.), and genes (e.g., atrogenes) have been identified as critical players in the regulation of muscle mass and atrophy and may play roles in the plasticity and vulnerability of muscle tissue under physiological and pathological conditions.

This Special Issue of Cells aims to provide a general overview of the cellular and molecular mechanisms responsible for muscle atrophy and to stimulate the identification of novel strategies to tackle conditions or disorders associated with muscle loss.

We look forward to your contributions.

Dr. Maria Pennuto
Dr. Marco Pirazzini
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • muscle atrophy
  • muscle proteostasis
  • muscle disuse
  • atrogenes
  • sarcopenia
  • neuromuscular disorder
  • myopathies
  • muscle degeneration
  • neuromuscular paralysis
  • cancer cachexia

Published Papers (1 paper)

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Research

Open AccessArticle
NeuroHeal Reduces Muscle Atrophy and Modulates Associated Autophagy
Cells 2020, 9(7), 1575; https://doi.org/10.3390/cells9071575 - 28 Jun 2020
Abstract
Muscle wasting is an unmet medical need which leads to a reduction of myofiber diameter and a negative impact on the functional performance of daily activities. We previously found that a new neuroprotective drug called NeuroHeal reduced muscle atrophy produced by transient denervation. [...] Read more.
Muscle wasting is an unmet medical need which leads to a reduction of myofiber diameter and a negative impact on the functional performance of daily activities. We previously found that a new neuroprotective drug called NeuroHeal reduced muscle atrophy produced by transient denervation. Aiming to decipher whether NeuroHeal has a direct role in muscle biology, we used herein different models of muscle atrophy: one caused by chronic denervation, another caused by hindlimb immobilization, and lastly, an in vitro model of myotube atrophy with Tumor Necrosis Factor-α (TNFα). In all these models, we observed that NeuroHeal reduced muscle atrophy and that SIRT1 activation seems to be required for that. The treatment downregulated some critical markers of protein degradation: Muscle Ring Finger 1 (MuRF1), K48 poly-Ub chains, and p62/SQSTM1. Moreover, it seems to restore the autophagy flux associated with denervation. Hence, we envisage a prospective use of NeuroHeal at clinics for different myopathies. Full article
(This article belongs to the Special Issue Skeletal Muscle Atrophy: Mechanisms at a Cellular Level)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Protein arginine methyltransferases in skeletal muscle and neuromuscular function
Authors: Jong-sun Kang
Affiliation: SungKyunKwan University, Suwon, South Korea

Title: Future use of myostatin – learning from the past
Authors: John Vissing
Affiliation: Department of Neurology, University of Copenhagen, Copenhagen, Denmark

Title: Insights into muscle atrophy from mass spectrometry profiling: Common properties of myocellular proteomes under stress
Authors: Siegfried Labeit
Affiliation: Medical Faculty Mannheim, University of Heidelberg, Germany

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