Special Issue "Skeletal Muscle Atrophy: Mechanisms at a Cellular Level"
Deadline for manuscript submissions: 1 September 2021.
Interests: neurodegenerative diseases; androgens; polyglutamine; metabolism; skeletal muscle
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
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.
- muscle atrophy
- muscle proteostasis
- muscle disuse
- neuromuscular disorder
- muscle degeneration
- neuromuscular paralysis
- cancer cachexia
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
Title: Small-molecule chemical knock-down of MuRF1 in melanoma bearing mice attenuates tumor cachexia associated myopathy
Authors: Volker Adams; Victoria Gußen; Sergey Zozulya; Andre Cruz; Anselmo Moriscot; Axel Linke; Siegfried Labeit
Affiliation: University of Heidelberg, Germany
Abstract: Patients with malignant tumors frequently suffer during disease progression from a syndrome referred to as cancer cachexia (CaCax): CaCax includes skeletal muscle atrophy and weakness, loss of body weight, and fat tissues. Currently, there are no FDA approved treatments available for CaCax. Here, we studied skeletal muscle atrophy and dysfunction in a murine CaCax model by injecting B16F10 melanoma cells into mouse thighs, and following mice during melanoma outgrowth. Skeletal muscles developed progressive weakness as detected by wire hang tests (WHTs) during days 13-23. Individual muscles analyzed at day 24 had atrophy, mitochondrial dysfunction, augmented metabolic ROS stress, and a catabolically activated UPS system, including upregulated MuRF1. Accordingly, we tested as an experimental intervention recently identified small molecules Myomed#205 and #946 that target the E3 ligase MuRF1. Results indicate that MuRF1 inhibitor feeding attenuated induction of MuRF1 in tumor stressed muscles. In addition, compounds augmented muscle performance in WHTs and attenuated muscle weight loss. Myomed#205 and #946 also rescued citrate synthase and succinate dehydrogenase levels in tumor-stressed muscles, possibly suggesting that metabolic and muscle wasting effects in this CaCax model are mechanistically connected. Inhibition of MuRF1 during tumor cachexia may represent a suitable strategy to attenuate skeletal muscle atrophy and dysfunction.
Title: Master regulators of muscle atrophy: role of costamere components
Authors: Luisa Gorza; Mara Brancaccio
Affiliation: Università degli Studi di Padova, Padua, Italy