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Cells
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Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities—Series...
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Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities—Series II

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

Deadline for manuscript submissions: closed (31 May 2024) | Viewed by 5660

Special Issue Editors

Prof. Dr. Antonio Musarò

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Guest Editor
Laboratory Affiliated to Istituto Pasteur Italia–Fondazione Cenci Bolognetti, DAHFMO-Unit of Histology and Medical Embryology, Sapienza University of Rome, Via A. Scarpa, 14, 00161 Rome, Italy
Interests: aging and neuromuscular diseases; role of stem cells and tissue niche on muscle regeneration; role of growth factors and cytokines in the physiopathology of skeletal muscle
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Graziella Messina

E-Mail Website
Guest Editor
Department of Biosciences, University of Milan, via Celoria 26, 20154 Milan, Italy
Interests: stem cells and regenerative medicine; cystic fibrosis; skeletal muscle development and regeneration; role of stem cells and tissue niche in the pathophysiology of cystic fibrosis and muscular dystrophies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is the expanded second edition of Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities that 1st edition resulted in the publishing of 24 papers and one Reprint Book.

The capacity of adult muscle to regenerate in response to injury stimuli represents an important homeostatic process. Regeneration is a highly coordinated program that partially recapitulates the embryonic developmental program, and involves the activation of the muscle compartment of stem cells, namely, satellite cells and other precursor cells, whose activity is strictly dependent on environmental signals. However, muscle regeneration is severely compromised in several pathological conditions due to either the progressive loss of stem cell populations or to missing signals that limit the damaged tissues from efficiently activating a regenerative program. It is therefore plausible that the loss of control over these cells’ fate might lead to pathological cell differentiation, limiting the ability of pathological muscle to sustain an efficient regenerative process. This Special Issue offers an open-access forum that aims to bring together a collection of original research and review articles addressing the intriguing field of the cellular and molecular players involved in muscle homeostasis and regeneration, and to suggest potential therapeutic approaches for degenerating muscle diseases. We hope to provide a stimulating resource for the fascinating subject of muscle research.

Prof. Dr. Antonio Musarò
Prof. Dr. Graziella Messina
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

  • muscle homeostasis
  • muscle regeneration
  • satellite cells
  • stem cells
  • FAPs
  • tissue niche
  • growth factors
  • inflammatory response
  • muscle pathology
  • aging

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Published Papers (3 papers)

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Research

22 pages, 5254 KiB  
Article
RhoA Is a Crucial Regulator of Myoblast Fusion
by Chiara Noviello, Kassandra Kobon, Voahangy Randrianarison-Huetz, Pascal Maire, France Pietri-Rouxel, Sestina Falcone and Athanassia Sotiropoulos
Cells 2023, 12(23), 2673; https://doi.org/10.3390/cells12232673 - 21 Nov 2023
Viewed by 1377
Abstract
Satellite cells (SCs) are adult muscle stem cells that are mobilized when muscle homeostasis is perturbed. Here we show that RhoA in SCs is indispensable to have correct muscle regeneration and hypertrophy. In particular, the absence of RhoA in SCs prevents a correct [...] Read more.
Satellite cells (SCs) are adult muscle stem cells that are mobilized when muscle homeostasis is perturbed. Here we show that RhoA in SCs is indispensable to have correct muscle regeneration and hypertrophy. In particular, the absence of RhoA in SCs prevents a correct SC fusion both to other RhoA-deleted SCs (regeneration context) and to growing control myofibers (hypertrophy context). We demonstrated that RhoA is dispensable for SCs proliferation and differentiation; however, RhoA-deleted SCs have an inefficient movement even if their cytoskeleton assembly is not altered. Proliferative myoblast and differentiated myotubes without RhoA display a decreased expression of Chordin, suggesting a crosstalk between these genes for myoblast fusion regulation. These findings demonstrate the importance of RhoA in SC fusion regulation and its requirement to achieve an efficient skeletal muscle homeostasis restoration. Full article
(This article belongs to the Special Issue Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities—Series II)
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20 pages, 3210 KiB  
Article
In Adult Skeletal Muscles, the Co-Receptors of Canonical Wnt Signaling, Lrp5 and Lrp6, Determine the Distribution and Size of Fiber Types, and Structure and Function of Neuromuscular Junctions
by Lea Gessler, Christopher Kurtek, Mira Merholz, Yongzhi Jian and Said Hashemolhosseini
Cells 2022, 11(24), 3968; https://doi.org/10.3390/cells11243968 - 8 Dec 2022
Cited by 4 | Viewed by 1959
Abstract
Canonical Wnt signaling is involved in skeletal muscle cell biology. The exact way in which this pathway exerts its contribution to myogenesis or neuromuscular junctions (NMJ) is a matter of debate. Next to the common co-receptors of canonical Wnt signaling, Lrp5 and Lrp6, [...] Read more.
Canonical Wnt signaling is involved in skeletal muscle cell biology. The exact way in which this pathway exerts its contribution to myogenesis or neuromuscular junctions (NMJ) is a matter of debate. Next to the common co-receptors of canonical Wnt signaling, Lrp5 and Lrp6, the receptor tyrosine kinase MuSK was reported to bind at NMJs WNT glycoproteins by its extracellular cysteine-rich domain. Previously, we reported canonical Wnt signaling being active in fast muscle fiber types. Here, we used conditional Lrp5 or Lrp6 knockout mice to investigate the role of these receptors in muscle cells. Conditional double knockout mice died around E13 likely due to ectopic expression of the Cre recombinase. Phenotypes of single conditional knockout mice point to a very divergent role for the two receptors. First, muscle fiber type distribution and size were changed. Second, canonical Wnt signaling reporter mice suggested less signaling activity in the absence of Lrps. Third, expression of several myogenic marker genes was changed. Fourth, NMJs were of fragmented phenotype. Fifth, recordings revealed impaired neuromuscular transmission. In sum, our data show fundamental differences in absence of each of the Lrp co-receptors and suggest a differentiated view of canonical Wnt signaling pathway involvement in adult skeletal muscle cells. Full article
(This article belongs to the Special Issue Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities—Series II)
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17 pages, 5300 KiB  
Article
In Skeletal Muscle Fibers, Protein Kinase Subunit CSNK2A1/CK2α Is Required for Proper Muscle Homeostasis and Structure and Function of Neuromuscular Junctions
by Mira Merholz, Yongzhi Jian, Johannes Wimberg, Lea Gessler and Said Hashemolhosseini
Cells 2022, 11(24), 3962; https://doi.org/10.3390/cells11243962 - 7 Dec 2022
Cited by 2 | Viewed by 1858
Abstract
CSNK2 tetrameric holoenzyme is composed of two subunits with catalytic activity (CSNK2A1 and/or CSNK2A2) and two regulatory subunits (CSNK2B) and is involved in skeletal muscle homeostasis. Up-to-date, constitutive Csnk2a2 knockout mice demonstrated mild regenerative impairments in skeletal muscles, while conditional Csnk2b mice were [...] Read more.
CSNK2 tetrameric holoenzyme is composed of two subunits with catalytic activity (CSNK2A1 and/or CSNK2A2) and two regulatory subunits (CSNK2B) and is involved in skeletal muscle homeostasis. Up-to-date, constitutive Csnk2a2 knockout mice demonstrated mild regenerative impairments in skeletal muscles, while conditional Csnk2b mice were linked to muscle weakness, impaired neuromuscular transmission, and metabolic and autophagic compromises. Here, for the first time, skeletal muscle-specific conditional Csnk2a1 mice were generated and characterized. The ablation of Csnk2a1 expression was ensured using a human skeletal actin-driven Cre reporter. In comparison with control mice, first, conditional knockout of CSNK2A1 resulted in age-dependent reduced grip strength. Muscle weakness was accompanied by impaired neuromuscular transmission. Second, the protein amount of other CSNK2 subunits was aberrantly changed. Third, the number of central nuclei in muscle fibers indicative of regeneration increased. Fourth, oxidative metabolism was impaired, reflected by an increase in cytochrome oxidase and accumulation of mitochondrial enzyme activity underneath the sarcolemma. Fifth, autophagic processes were stimulated. Sixth, NMJs were fragmented and accompanied by increased synaptic gene expression levels. Altogether, knockout of Csnk2a1 or Csnk2b results in diverse impairments of skeletal muscle biology. Full article
(This article belongs to the Special Issue Muscle Homeostasis and Regeneration: From Molecular Mechanisms to Therapeutic Opportunities—Series II)
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