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Biomolecules
Special Issues
State of the Art of Myology in 2024
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State of the Art of Myology in 2024

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 1328

Special Issue Editors

Prof. Dr. Guglielmo Sorci

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Perugia, 06132 Perugia, Italy
Interests: myogenesis; satellite cells; muscle regeneration; muscular dystrophy; sarcopenia; cancer cachexia; rhabdomyosarcoma; S100B; RAGE (receptor for advanced glycation end-products)
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Francesca Riuzzi

E-Mail Website
Guest Editor
Department Medicine and Surgery, University of Perugia, 06132 Perugia, Italy
Interests: muscle precursor cells; muscle regeneration; sarcopenia; cancer cachexia; muscular dystrophy; natural compounds; HMGB1; RAGE (receptor for advanced glycation end-products)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of the state of the art of myology. We invite research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and systematic reviews. Potential topics include, but are not limited to, the following research areas:

  • Embryonic myogenesis;
  • Adult myogenesis;
  • Exercise-induced muscle injury;
  • Muscular dystrophies and muscle diseases;
  • Sarcopenia;
  • Cachexia;
  • Rhabdomyosarcoma;
  • Muscle biophysics.

Prof. Dr. Guglielmo Sorci
Prof. Dr. Francesca Riuzzi
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. Biomolecules 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 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

  • embryonic myogenesis
  • adult myogenesis
  • exercise-induced muscle injury
  • muscular dystrophies and muscle diseases
  • sarcopenia
  • cachexia
  • rhabdomyosarcoma
  • muscle biophysics

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Published Papers (2 papers)

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Research

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16 pages, 6419 KiB  
Article
Phospholipase Cδ-4 (PLCδ4) Acts as a Nuclear Player to Influence Cyclin B Expression in the Embryonal Rhabdomyosarcoma Cell Lines RD and A204
by Sara Salucci, Alberto Bavelloni, Ilaria Versari, Sabrina Burattini, Francesco Bavelloni, Pietro Gobbi, Alessandro Fanzani, Silvia Codenotti, William Blalock, Katia Scotlandi and Irene Faenza
Biomolecules 2024, 14(9), 1180; https://doi.org/10.3390/biom14091180 - 20 Sep 2024
Viewed by 213
Abstract
Rhabdomyosarcoma (RMS), the most common form of sarcoma typical of pediatric age, arises from the malignant transformation of the mesenchymal precursors that fail to differentiate into skeletal muscle cells. Here, we investigated whether the protein phospholipase C δ4 (PLCδ4), a member of the [...] Read more.
Rhabdomyosarcoma (RMS), the most common form of sarcoma typical of pediatric age, arises from the malignant transformation of the mesenchymal precursors that fail to differentiate into skeletal muscle cells. Here, we investigated whether the protein phospholipase C δ4 (PLCδ4), a member of the PLC family involved in proliferation and senescence mechanisms of mesenchymal stromal stem cells, may play a role in RMS. Our molecular and morpho-functional data reveal that PLCδ4 is highly expressed in the fusion-negative, p53-positive, SMARCB1 heterozygous mutated embryonal RMS (ERMS) cell line A204, while it is poorly expressed in the ERMS cell lines RD (fusion-negative, MYC amplification, N-RAS (Q61H), homozygous mutated p53) and Hs729 (homozygous mutated p53) and the alveolar rhabdosarcoma (ARMS) cell line SJCRH30 (RH30; fusion positive, heterozygous mutated RARA, polyheterozygous mutated p53). To characterize the role of PLCδ4, the RD cell line was stably transfected with wild-type PLCδ4 (RD/PLCδ4). Overexpressed PLCδ4 mainly localized to the nucleus in RD cells and contributed to the phosphorylation of PRAS40 (T246), Chk2(T68), WNK1(T60), and Akt 1/273 (S473), as revealed by proteome profiler array analysis. Overexpression of PLCδ4 in RD cells enhanced cyclin B1 expression and resulted in G2/M-phase cell cycle arrest. In contrast, siRNA-mediated knockdown of PLCδ4 in A204 cells resulted in reduced cyclin B1 expression. Our study identifies a novel role for nuclear PLCδ4 as a regulator of cyclin B1 via Akt-dependent phosphorylation. The modulation of PLCδ4 expression and its downstream targets could represent a crucial signaling pathway to block embryonal RMS cell proliferation. Full article
(This article belongs to the Special Issue State of the Art of Myology in 2024)
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Review

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19 pages, 1688 KiB  
Review
Current Treatment Methods for Charcot–Marie–Tooth Diseases
by Hongxian Dong, Boquan Qin, Hui Zhang, Lei Lei and Shizhou Wu
Biomolecules 2024, 14(9), 1138; https://doi.org/10.3390/biom14091138 - 9 Sep 2024
Viewed by 739
Abstract
Charcot–Marie–Tooth (CMT) disease, the most common inherited neuromuscular disorder, exhibits a wide phenotypic range, genetic heterogeneity, and a variable disease course. The diverse molecular genetic mechanisms of CMT were discovered over the past three decades with the development of molecular biology and gene [...] Read more.
Charcot–Marie–Tooth (CMT) disease, the most common inherited neuromuscular disorder, exhibits a wide phenotypic range, genetic heterogeneity, and a variable disease course. The diverse molecular genetic mechanisms of CMT were discovered over the past three decades with the development of molecular biology and gene sequencing technologies. These methods have brought new options for CMT reclassification and led to an exciting era of treatment target discovery for this incurable disease. Currently, there are no approved disease management methods that can fully cure patients with CMT, and rehabilitation, orthotics, and surgery are the only available treatments to ameliorate symptoms. Considerable research attention has been given to disease-modifying therapies, including gene silencing, gene addition, and gene editing, but most treatments that reach clinical trials are drug treatments, while currently, only gene therapies for CMT2S have reached the clinical trial stage. In this review, we highlight the pathogenic mechanisms and therapeutic investigations of different subtypes of CMT, and promising therapeutic approaches are also discussed. Full article
(This article belongs to the Special Issue State of the Art of Myology in 2024)
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