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Cells
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Recent Research on Muscle Homeostasis and Regeneration
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Recent Research on Muscle Homeostasis and Regeneration

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 7421

Special Issue Editor

Dr. Giulia Maria Camerino

E-Mail Website
Guest Editor
Department of Pharmacy-Drug Sciences, University of Bari Aldo Moro, 70125 Bari, Italy
Interests: pharmacology; skeletal muscle; muscle homeostasis; cachexia; muscle disuse; muscles disease; rare diseases; iatrogenic diseases; muscle brain crosstalk; neurodegeneration; neurons

Special Issue Information

Dear Colleagues,

The capacity of adult muscle to regenerate in response to injury stimuli represents an important homeostatic process. Muscle regeneration is crucial for adult skeletal muscle, which, after development, retains the capacity to regenerate in response to appropriate stimuli, activating the muscle compartment of satellite cells. The myogenic program must be highly coordinated to favor the birth of new fibers. The initial phase of muscle repair is characterized by necrosis of the damaged tissue and activation of an inflammatory response. This phase is followed by the activation of myogenic cells to proliferate, differentiate, and fuse, leading to new myofiber. Muscle regeneration is severely modified 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.

This Special Issue aims to provide original research addressing the theme of the “Muscle Homeostasis and Regeneration”, including, but not limited to: cellular and molecular players involved in muscle homeostasis and regeneration, new evidence on the physiological and pathological conditions related to muscle regenerations, and new information about potential therapeutic approaches for degenerating muscle diseases.

Dr. Giulia Maria Camerino
Guest Editor

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
  • growth factors
  • inflammatory response
  • muscle pathology

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Published Papers (3 papers)

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Research

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19 pages, 3552 KiB  
Article
Tumor Necrosis Factor-Alpha Modulates Expression of Genes Involved in Cytokines and Chemokine Pathways in Proliferative Myoblast Cells
by Angela María Alvarez, Carlos Eduardo Madureira Trufen, Marcus Vinicius Buri, Marcela Bego Nering de Sousa, Francisco Ivanio Arruda-Alves, Flavio Lichtenstein, Ursula Castro de Oliveira, Inácio de Loiola Meirelles Junqueira-de-Azevedo, Catarina Teixeira and Vanessa Moreira
Cells 2024, 13(13), 1161; https://doi.org/10.3390/cells13131161 - 8 Jul 2024
Cited by 2 | Viewed by 1877
Abstract
Skeletal muscle regeneration after injury is a complex process involving inflammatory signaling and myoblast activation. Pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) are key mediators, but their effects on gene expression in proliferating myoblasts are unclear. We performed the RNA sequencing of TNF-α [...] Read more.
Skeletal muscle regeneration after injury is a complex process involving inflammatory signaling and myoblast activation. Pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) are key mediators, but their effects on gene expression in proliferating myoblasts are unclear. We performed the RNA sequencing of TNF-α treated C2C12 myoblasts to elucidate the signaling pathways and gene networks regulated by TNF-α during myoblast proliferation. The TNF-α (10 ng/mL) treatment of C2C12 cells led to 958 differentially expressed genes compared to the controls. Pathway analysis revealed significant regulation of TNF-α signaling, along with the chemokine and IL-17 pathways. Key upregulated genes included cytokines (e.g., IL-6), chemokines (e.g., CCL7), and matrix metalloproteinases (MMPs). TNF-α increased myogenic factor 5 (Myf5) but decreased MyoD protein levels and stimulated the release of MMP-9, MMP-10, and MMP-13. TNF-α also upregulates versican and myostatin mRNA. Overall, our study demonstrates the TNF-α modulation of distinct gene expression patterns and signaling pathways that likely contribute to enhanced myoblast proliferation while suppressing premature differentiation after muscle injury. Elucidating the mechanisms involved in skeletal muscle regeneration can aid in the development of regeneration-enhancing therapeutics. Full article
(This article belongs to the Special Issue Recent Research on Muscle Homeostasis and Regeneration)
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13 pages, 2774 KiB  
Communication
AMPK Phosphorylation Impacts Apoptosis in Differentiating Myoblasts Isolated from Atrophied Rat Soleus Muscle
by Natalia A. Vilchinskaya, Sergey V. Rozhkov, Olga V. Turtikova, Timur M. Mirzoev and Boris S. Shenkman
Cells 2023, 12(6), 920; https://doi.org/10.3390/cells12060920 - 16 Mar 2023
Cited by 7 | Viewed by 2158
Abstract
Regrowth of atrophied myofibers depends on muscle satellite cells (SCs) that exist outside the plasma membrane. Muscle atrophy appears to result in reduced number of SCs due to apoptosis. Given reduced AMP-activated protein kinase (AMPK) activity during differentiation of primary myoblasts derived from [...] Read more.
Regrowth of atrophied myofibers depends on muscle satellite cells (SCs) that exist outside the plasma membrane. Muscle atrophy appears to result in reduced number of SCs due to apoptosis. Given reduced AMP-activated protein kinase (AMPK) activity during differentiation of primary myoblasts derived from atrophic muscle, we hypothesized that there may be a potential link between AMPK and susceptibility of differentiating myoblasts to apoptosis. The aim of this study was to estimate the effect of AMPK activation (via AICAR treatment) on apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle. Thirty rats were randomly assigned to the following two groups: control (C, n = 10) and 7-day hindlimb suspension (HS, n = 20). Myoblasts derived from the soleus muscles of HS rats were divided into two parts: AICAR-treated cells and non-treated cells. Apoptotic processes were evaluated by using TUNEL assay, RT-PCR and WB. In differentiating myoblasts derived from the atrophied soleus, there was a significant decrease (p < 0.05) in AMPK and ACC phosphorylation in parallel with increased number of apoptotic nuclei and a significant upregulation of pro-apoptotic markers (caspase-3, -9, BAX, p53) compared to the cells derived from control muscles. AICAR treatment of atrophic muscle-derived myoblasts during differentiation prevented reductions in AMPK and ACC phosphorylation as well as maintained the number of apoptotic nuclei and the expression of pro-apoptotic markers at the control levels. Thus, the maintenance of AMPK activity can suppress enhanced apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle. Full article
(This article belongs to the Special Issue Recent Research on Muscle Homeostasis and Regeneration)
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Review

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30 pages, 1917 KiB  
Review
Tripartite Motif-Containing Protein 32 (TRIM32): What Does It Do for Skeletal Muscle?
by Seung Yeon Jeong, Jun Hee Choi, Jooho Kim, Jin Seok Woo and Eun Hui Lee
Cells 2023, 12(16), 2104; https://doi.org/10.3390/cells12162104 - 19 Aug 2023
Cited by 6 | Viewed by 2699
Abstract
Tripartite motif-containing protein 32 (TRIM32) is a member of the tripartite motif family and is highly conserved from flies to humans. Via its E3 ubiquitin ligase activity, TRIM32 mediates and regulates many physiological and pathophysiological processes, such as growth, differentiation, muscle regeneration, immunity, [...] Read more.
Tripartite motif-containing protein 32 (TRIM32) is a member of the tripartite motif family and is highly conserved from flies to humans. Via its E3 ubiquitin ligase activity, TRIM32 mediates and regulates many physiological and pathophysiological processes, such as growth, differentiation, muscle regeneration, immunity, and carcinogenesis. TRIM32 plays multifunctional roles in the maintenance of skeletal muscle. Genetic variations in the TRIM32 gene are associated with skeletal muscular dystrophies in humans, including limb–girdle muscular dystrophy type 2H (LGMD2H). LGMD2H-causing genetic variations of TRIM32 occur most frequently in the C-terminal NHL (ncl-1, HT2A, and lin-41) repeats of TRIM32. LGMD2H is characterized by skeletal muscle dystrophy, myopathy, and atrophy. Surprisingly, most patients with LGMD2H show minimal or no dysfunction in other tissues or organs, despite the broad expression of TRIM32 in various tissues. This suggests more prominent roles for TRIM32 in skeletal muscle than in other tissues or organs. This review is focused on understanding the physiological roles of TRIM32 in skeletal muscle, the pathophysiological mechanisms mediated by TRIM32 genetic variants in LGMD2H patients, and the correlations between TRIM32 and Duchenne muscular dystrophy (DMD). Full article
(This article belongs to the Special Issue Recent Research on Muscle Homeostasis and Regeneration)
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