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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (29 November 2023) | Viewed by 8701

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Dr. Federica Cirillo

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Guest Editor

1. IRCCS Policlinico San Donato, 20097 San Donato Milanese, MI, Italy
2. Institute for Molecular and Translational Cardiology (IMTC), 20097 San Donato Milanese, MI, Italy
Interests: muscle regenation; hypoxia; muscle metabolism; sarcopenia; myogenesis

Dr. Giorgia Careccia

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Guest Editor

Department of Biosciences, University of Milan, 20133 Milan, Italy
Interests: myogenesis; muscular dystrophies; stem cells; inflammation; regeneration

Prof. Dr. Laura Mangiavini

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Guest Editor

1. Department of Biomedical Sciences for Health, University of Milan, 20133 Milan, Italy
2. IRCCS Ospedale Galeazzi Sant’Ambrogio, 20157 Milan, Italy
Interests: knee arthroplasty; knee osteoarthritis; sarcopenia; bone and cartilage development; tissue engineering strategies for musculoskeletal tissues
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Special Issue Information

Dear Colleagues,

The skeletal muscle is the most abundant tissue in mammals and is responsible for voluntary movement. Myogenesis is the process that leads to the formation of multinucleated and contractile myofibers during development and regeneration after damage. Satellite cells (SCs), the skeletal muscle stem cells, are crucial players in casting the (re-)generation of skeletal muscle. Alterations in the number and functions of SCs have been associated with muscular dystrophies and sarcopenia, but without a complete understanding of the molecular mechanism and with critical problems in finding effective treatments. Deciphering the role of SCs alterations (and myogenesis) may be crucial for developing efficient therapeutic strategies for various muscular diseases.

This Special Issue entitled "Myogenesis and Muscular Disorders" will comprise articles and reviews related to, but not limited to, the following topics:

Myogenesis and SCs modulation in muscular diseases.
Novel targets involved in (transcriptional, post-transcriptional, and post-translational) regulation of muscle regeneration.
Use of small molecules to activate SCs.
Role of SCs (metabolism) in the development of muscle diseases.
Effects of nutrients, hormones, and exercise on promoting muscle regeneration.
Modulation of the inflammatory response as a potential therapeutic strategy to counteract the loss of SCs.
Efficacy of combined pharmacological and cognitive-behavioral therapies.

Dr. Federica Cirillo
Dr. Giorgia Careccia
Prof. Dr. Laura Mangiavini
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

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Research

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16 pages, 2524 KiB

Open AccessArticle

All-Trans Retinoic Acid-Responsive LGR6 Is Transiently Expressed during Myogenic Differentiation and Is Required for Myoblast Differentiation and Fusion

by Tomoya Kitakaze, Rina Tatsumi, Mayu Yamaguchi, Aino Nakatsuji, Naoki Harada and Ryoichi Yamaji

Int. J. Mol. Sci. 2023, 24(10), 9035; https://doi.org/10.3390/ijms24109035 - 20 May 2023

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Abstract

All-trans retinoic acid (ATRA) promotes myoblast differentiation into myotubes. Leucine-rich repeat-containing G-protein-coupled receptor 6 (LGR6) is a candidate ATRA-responsive gene; however, its role in skeletal muscles remains unclear. Here, we demonstrated that during the differentiation of murine C2C12 myoblasts into myotubes, Lgr6 mRNA expression transiently increased before the increase in the expression of the mRNAs encoding myogenic regulatory factors, such as myogenin, myomaker, and myomerger. The loss of LGR6 decreased the differentiation and fusion indices. The exogenous expression of LGR6 up to 3 and 24 h after the induction of differentiation increased and decreased the mRNA levels of myogenin, myomaker, and myomerger, respectively. Lgr6 mRNA was transiently expressed after myogenic differentiation in the presence of a retinoic acid receptor α (RARα) agonist and an RARγ agonist in addition to ATRA, but not in the absence of ATRA. Furthermore, a proteasome inhibitor or Znfr3 knockdown increased exogenous LGR6 expression. The loss of LGR6 attenuated the Wnt/β-catenin signaling activity induced by Wnt3a alone or in combination with Wnt3a and R-spondin 2. These results indicate that LGR6 promotes myogenic differentiation and that ATRA is required for the transient expression of LGR6 during differentiation. Furthermore, LGR6 expression appeared to be downregulated by the ubiquitin–proteasome system involving ZNRF3. Full article

(This article belongs to the Special Issue Myogenesis and Muscular Diseases)

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15 pages, 3463 KiB

Open AccessArticle

Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation

by Izumi Matsuba, Rikako Fujita and Kaoruko Iida

Int. J. Mol. Sci. 2023, 24(6), 5847; https://doi.org/10.3390/ijms24065847 - 19 Mar 2023

Cited by 2 | Viewed by 2500

Abstract

Sarcopenia associated with aging and obesity is characterized by the atrophy of fast-twitch muscle fibers and an increase in intramuscular fat deposits. However, the mechanism of fast-twitch fiber-specific atrophy remains unclear. In this study, we aimed to assess the effect of palmitic acid (PA), the most common fatty acid component of human fat, on muscle fiber type, focusing on the expression of fiber-type-specific myosin heavy chain (MHC). Myotubes differentiated from C2C12 myoblasts were treated with PA. The PA treatment inhibited myotube formation and hypertrophy while reducing the gene expression of MHC IIb and IIx, specific isoforms of fast-twitch fibers. Consistent with this, a significant suppression of MHC IIb protein expression in PA-treated cells was observed. A reporter assay using plasmids containing the MHC IIb gene promoter revealed that the PA-induced reduction in MHC IIb gene expression was caused by the suppression of MyoD transcriptional activity through its phosphorylation. Treatment with a specific protein kinase C (PKC) inhibitor recovered the reduction in MHC IIb gene expression levels in PA-treated cells, suggesting the involvement of the PA-induced activation of PKC. Thus, PA selectively suppresses the mRNA and protein expression of fast-twitch MHC by modulating MyoD activity. This finding provides a potential pathogenic mechanism for age-related sarcopenia. Full article

(This article belongs to the Special Issue Myogenesis and Muscular Diseases)

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Review

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24 pages, 1390 KiB

Open AccessReview

Regulation of Satellite Cells Functions during Skeletal Muscle Regeneration: A Critical Step in Physiological and Pathological Conditions

by Giorgia Careccia, Laura Mangiavini and Federica Cirillo

Int. J. Mol. Sci. 2024, 25(1), 512; https://doi.org/10.3390/ijms25010512 - 29 Dec 2023

Cited by 2 | Viewed by 1969

Abstract

Skeletal muscle regeneration is a complex process involving the generation of new myofibers after trauma, competitive physical activity, or disease. In this context, adult skeletal muscle stem cells, also known as satellite cells (SCs), play a crucial role in regulating muscle tissue homeostasis and activating regeneration. Alterations in their number or function have been associated with various pathological conditions. The main factors involved in the dysregulation of SCs’ activity are inflammation, oxidative stress, and fibrosis. This review critically summarizes the current knowledge on the role of SCs in skeletal muscle regeneration. It examines the changes in the activity of SCs in three of the most common and severe muscle disorders: sarcopenia, muscular dystrophy, and cancer cachexia. Understanding the molecular mechanisms involved in their dysregulations is essential for improving current treatments, such as exercise, and developing personalized approaches to reactivate SCs. Full article

(This article belongs to the Special Issue Myogenesis and Muscular Diseases)

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21 pages, 778 KiB

Open AccessReview

PAX7, a Key for Myogenesis Modulation in Muscular Dystrophies through Multiple Signaling Pathways: A Systematic Review

by Nor Idayu A. Rahman, Chung Liang Lam, Nadiah Sulaiman, Nur Atiqah Haizum Abdullah, Fazlina Nordin, Shahrul Hisham Zainal Ariffin and Muhammad Dain Yazid

Int. J. Mol. Sci. 2023, 24(17), 13051; https://doi.org/10.3390/ijms241713051 - 22 Aug 2023

Cited by 2 | Viewed by 1959

Abstract

Muscular dystrophy is a heterogenous group of hereditary muscle disorders caused by mutations in the genes responsible for muscle development, and is generally defined by a disastrous progression of muscle wasting and massive loss in muscle regeneration. Pax7 is closely associated with myogenesis, which is governed by various signaling pathways throughout a lifetime and is frequently used as an indicator in muscle research. In this review, an extensive literature search adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was performed to identify research that examined signaling pathways in living models, while quantifying Pax7 expression in myogenesis. A total of 247 articles were retrieved from the Web of Science (WoS), PubMed and Scopus databases and were thoroughly examined and evaluated, resulting in 19 articles which met the inclusion criteria. Admittedly, we were only able to discuss the quantification of Pax7 carried out in research affecting various type of genes and signaling pathways, rather than the expression of Pax7 itself, due to the massive differences in approach, factor molecules and signaling pathways analyzed across the research. However, we highlighted the thorough evidence for the alteration of the muscle stem cell precursor Pax7 in multiple signaling pathways described in different living models, with an emphasis on the novel approach that could be taken in manipulating Pax7 expression itself in dystrophic muscle, towards the discovery of an effective treatment for muscular dystrophy. Therefore, we believe that this could be applied to the potential gap in muscle research that could be filled by tuning the well-established marker expression to improve dystrophic muscle. Full article

(This article belongs to the Special Issue Myogenesis and Muscular Diseases)

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