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Signalling Pathways in Striated Muscle Differentiation, Histogenesis and Repair

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 2369

Special Issue Editors

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Guest Editor
Department of Anatomical, Histological, Forensic Medicine and Orthopedic Sciences (DAHFMO), Sapienza University of Rome, Rome, Italy
Interests: striated muscles; muscle diseases; muscle immunology; intercellular communication
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Unit of Histology and Medical Embryology, Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Sapienza University of Rome, 00185 Rome, Italy
Interests: muscle differentiation and histogenesis; muscle regeneration and remodelling; satellite cells; intracellular signalling; protein kinase C; muscular dystrophies; immune response

Special Issue Information

Dear Colleagues,

This Special Issue aims to bring together recent and current research associated with signaling pathways regulating striated muscle differentiation, histogenesis, and remodeling. This is a re-edition of a previous issue published in 2020, but with a broader focus on both skeletal and cardiac (striated) muscle, taking into account the fact that both tissues undergo changes in response to similar physiological or pathological stimuli. Indeed, both muscles are dynamic tissues capable of responding to a large variety of stimuli by adjusting muscle growth, size, metabolism, and function. Numerous recent studies have expanded our knowledge of the complexity of the signaling pathways regulating these processes. Indeed, it is becoming clear that a precisely regulated process, involving endocrine/paracrine and cell–cell contact interactions, is required for the maintenance of muscle homeostasis. Alterations of these mechanisms lead to unsuccessful repair in response to direct mechanical trauma (acute injury) or following secondary damage because of aging or genetic defects. Striated muscle biology is studied from many different viewpoints: genetic diseases, sports medicine, physiology, immunology, developmental biology, gene regulation, and regeneration. In recent years, advances in our understanding of the mechanisms of muscle diseases and disfunctions have led to a major focus on translational research and pharmacological therapies for clinically important muscle pathologies. The focus of this Special Issue is to bring together studies that use different experimental approaches in vivo or in vitro to dissect the dynamic changes taking place in muscle building and maintenance, and their contribution to normal versus pathological muscle repair. 

Prof. Dr. Marina Bouché
Dr. Biliana Lozanoska-Ochser
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.


  • signaling pathways
  • skeletal muscle
  • cardiac muscle
  • muscle development
  • muscle homeostasis
  • muscle atrophy
  • muscular dystrophies
  • satellite cells
  • tissue regeneration
  • inflammation

Published Papers (1 paper)

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16 pages, 3330 KiB  
Inhibition of PKCθ Improves Dystrophic Heart Phenotype and Function in a Novel Model of DMD Cardiomyopathy
by Jacopo Morroni, Leonardo Schirone, Valentina Valenti, Clemens Zwergel, Carles Sánchez Riera, Sergio Valente, Daniele Vecchio, Sonia Schiavon, Rino Ragno, Antonello Mai, Sebastiano Sciarretta, Biliana Lozanoska-Ochser and Marina Bouchè
Int. J. Mol. Sci. 2022, 23(4), 2256; https://doi.org/10.3390/ijms23042256 - 18 Feb 2022
Cited by 1 | Viewed by 1968
Chronic cardiac muscle inflammation and subsequent fibrotic tissue deposition are key features in Duchenne Muscular Dystrophy (DMD). The treatment of choice for delaying DMD progression both in skeletal and cardiac muscle are corticosteroids, supporting the notion that chronic inflammation in the heart plays [...] Read more.
Chronic cardiac muscle inflammation and subsequent fibrotic tissue deposition are key features in Duchenne Muscular Dystrophy (DMD). The treatment of choice for delaying DMD progression both in skeletal and cardiac muscle are corticosteroids, supporting the notion that chronic inflammation in the heart plays a pivotal role in fibrosis deposition and subsequent cardiac dysfunction. Nevertheless, considering the adverse effects associated with long-term corticosteroid treatments, there is a need for novel anti-inflammatory therapies. In this study, we used our recently described exercised mdx (ex mdx) mouse model characterised by accelerated heart pathology, and the specific PKCθ inhibitor Compound 20 (C20), to show that inhibition of this kinase leads to a significant reduction in the number of immune cells infiltrating the heart, as well as necrosis and fibrosis. Functionally, C20 treatment also prevented the reduction in left ventricle fractional shortening, which was typically observed in the vehicle-treated ex mdx mice. Based on these findings, we propose that PKCθ pharmacological inhibition could be an attractive therapeutic approach to treating dystrophic cardiomyopathy Full article
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