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Cells
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Autophagy and Apoptosis in Skeletal Muscle
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Autophagy and Apoptosis in Skeletal Muscle

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 4794

Special Issue Editors

Dr. Cristiana Perrotta

E-Mail Website
Guest Editor
Department of Biomedical and Clinical Sciences, Università degli Studi di Milano, Milan, Italy
Interests: apoptosis; muscular dystrophy; immune system; sphingolipids
Dr. Clara De Palma

E-Mail Website
Guest Editor
Department of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy
Interests: mitochondria; skeletal muscle; autophagy; muscular dystrophy; metabolism
Prof. Claudia Moscheni

E-Mail Website
Guest Editor
Department of Biomedical and Clinical Sciences, Università degli Studi di Milano, Milan, Italy
Interests: mitochondria; autophagy; extracellular matrix; electron microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy and apoptosis are two key processes for maintaining cellular homeostasis in tissues and are regulated through various and highly coordinated signal transduction mechanisms.

Also in skeletal muscle, a plastic tissue that reacts and adjusts to several physiological and pathological conditions, autophagy and apoptosis are finely tuned and may have both beneficial and harmful effects, depending on the condition of the tissue and their level of activation. For instance, both processes may impinge the fate of skeletal muscle after damage and contribute to the pathogenesis of diseases such as myopathies and muscular dystrophies.

In this Special Issue, we will collect studies focused on the role of autophagy and/or apoptosis in skeletal muscle homeostasis, injury, and repair and in skeletal muscle diseases such as myopathies, muscular dystrophies, atrophy, and sarcopenia, also focusing on the interaction with immune system cells. Furthermore, we encourage research on mitophagy and mitochondrial apoptotic signaling in skeletal muscle pathophysiology, due to mitochondria’s critical role in determining cell life and death. Finally, we aim to gather studies exploring the possibility of targeting autophagy/apoptosis as novel therapeutic strategies for the treatment of muscle diseases. Original research papers, review articles, communications, perspectives, and commentaries are welcome.

Dr. Cristiana Perrotta
Dr. Clara De Palma
Dr. Claudia Moscheni
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 submissions that pass pre-check are 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 semimonthly 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 2700 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

  • autophagy
  • apoptosis
  • skeletal muscle
  • cell signaling
  • mitochondria
  • myopathies
  • sarcopenia
  • atrophy
  • immune system
  • therapeutic strategies

Published Papers (2 papers)

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Review

17 pages, 1310 KiB  
Review
Mitochondria and Reactive Oxygen Species: The Therapeutic Balance of Powers for Duchenne Muscular Dystrophy
by Silvia Rosanna Casati, Davide Cervia, Paulina Roux-Biejat, Claudia Moscheni, Cristiana Perrotta and Clara De Palma
Cells 2024, 13(7), 574; https://doi.org/10.3390/cells13070574 - 26 Mar 2024
Viewed by 1101
Abstract
Duchenne muscular dystrophy (DMD) is a genetic progressive muscle-wasting disorder that leads to rapid loss of mobility and premature death. The absence of functional dystrophin in DMD patients reduces sarcolemma stiffness and increases contraction damage, triggering a cascade of events leading to muscle [...] Read more.
Duchenne muscular dystrophy (DMD) is a genetic progressive muscle-wasting disorder that leads to rapid loss of mobility and premature death. The absence of functional dystrophin in DMD patients reduces sarcolemma stiffness and increases contraction damage, triggering a cascade of events leading to muscle cell degeneration, chronic inflammation, and deposition of fibrotic and adipose tissue. Efforts in the last decade have led to the clinical approval of novel drugs for DMD that aim to restore dystrophin function. However, combination therapies able to restore dystrophin expression and target the myriad of cellular events found impaired in dystrophic muscle are desirable. Muscles are higher energy consumers susceptible to mitochondrial defects. Mitochondria generate a significant source of reactive oxygen species (ROS), and they are, in turn, sensitive to proper redox balance. In both DMD patients and animal models there is compelling evidence that mitochondrial impairments have a key role in the failure of energy homeostasis. Here, we highlighted the main aspects of mitochondrial dysfunction and oxidative stress in DMD and discussed the recent findings linked to mitochondria/ROS-targeted molecules as a therapeutic approach. In this respect, dual targeting of both mitochondria and redox homeostasis emerges as a potential clinical option in DMD. Full article
(This article belongs to the Special Issue Autophagy and Apoptosis in Skeletal Muscle)
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25 pages, 1629 KiB  
Review
The Role of Mitophagy in Skeletal Muscle Damage and Regeneration
by Eirini Chatzinikita, Maria Maridaki, Konstantinos Palikaras, Michael Koutsilieris and Anastassios Philippou
Cells 2023, 12(5), 716; https://doi.org/10.3390/cells12050716 - 24 Feb 2023
Cited by 7 | Viewed by 3207
Abstract
Mitochondria are cellular organelles that play an essential role in generating the chemical energy needed for the biochemical reactions in cells. Mitochondrial biogenesis, i.e., de novo mitochondria formation, results in enhanced cellular respiration, metabolic processes, and ATP generation, while autophagic clearance of mitochondria [...] Read more.
Mitochondria are cellular organelles that play an essential role in generating the chemical energy needed for the biochemical reactions in cells. Mitochondrial biogenesis, i.e., de novo mitochondria formation, results in enhanced cellular respiration, metabolic processes, and ATP generation, while autophagic clearance of mitochondria (mitophagy) is required to remove damaged or useless mitochondria. The balance between the opposing processes of mitochondrial biogenesis and mitophagy is highly regulated and crucial for the maintenance of the number and function of mitochondria as well as for the cellular homeostasis and adaptations to metabolic demands and extracellular stimuli. In skeletal muscle, mitochondria are essential for maintaining energy homeostasis, and the mitochondrial network exhibits complex behaviors and undergoes dynamic remodeling in response to various conditions and pathologies characterized by changes in muscle cell structure and metabolism, such as exercise, muscle damage, and myopathies. In particular, the involvement of mitochondrial remodeling in mediating skeletal muscle regeneration following damage has received increased attention, as modifications in mitophagy-related signals arise from exercise, while variations in mitochondrial restructuring pathways can lead to partial regeneration and impaired muscle function. Muscle regeneration (through myogenesis) following exercise-induced damage is characterized by a highly regulated, rapid turnover of poor-functioning mitochondria, permitting the synthesis of better-functioning mitochondria to occur. Nevertheless, essential aspects of mitochondrial remodeling during muscle regeneration remain poorly understood and warrant further characterization. In this review, we focus on the critical role of mitophagy for proper muscle cell regeneration following damage, highlighting the molecular mechanisms of the mitophagy-associated mitochondrial dynamics and network reformation. Full article
(This article belongs to the Special Issue Autophagy and Apoptosis in Skeletal Muscle)
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