Skeletal Muscle: Structure, Physiology and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 186

Special Issue Editor


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Guest Editor
Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy
Interests: cellular and molecular muscle biology; myogenesis; genetics of muscle diseases; muscular dystrophy; excitation contraction coupling; malignant hyperthermia; molecular and cellular biology; skeletal muscle physiology; skeletal muscle metabolism
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Special Issue Information

Dear Colleagues,

Skeletal muscle is the most abundant tissue in mammals, accounting for a significant portion of the total body mass of healthy individuals. Its structure and function are intricately connected. Skeletal muscle plays a critical role in contraction, enabling movement, supporting body posture and position, and maintaining body temperature. These functions place high metabolic demands on skeletal muscle, highlighting its critical role in body metabolism. Needless to say, any alteration in one of the skeletal muscle components can lead to disease.

This Special Issue invites manuscripts that provide insights into recent developments in skeletal muscle structure, physiology, and diseases. Submissions can include both research papers and review articles from diverse disciplines such as biophysics, cell biology, molecular biology, and genetics.

Prof. Dr. Vincenzo Sorrentino
Guest Editor

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Keywords

  • excitation–contraction coupling
  • store-operated calcium entry
  • sarcomeric proteins
  • skeletal muscle metabolism
  • skeletal muscle diseases
  • muscle plasticity
  • development
  • sarcopenia
  • aging

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Published Papers (1 paper)

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Research

28 pages, 11365 KiB  
Article
Multi-Modal Analysis of Satellite Cells Reveals Early Impairments at Pre-Contractile Stages of Myogenesis in Duchenne Muscular Dystrophy
by Sophie Franzmeier, Shounak Chakraborty, Armina Mortazavi, Jan B. Stöckl, Jianfei Jiang, Nicole Pfarr, Benedikt Sabass, Thomas Fröhlich, Clara Kaufhold, Michael Stirm, Eckhard Wolf, Jürgen Schlegel and Kaspar Matiasek
Cells 2025, 14(12), 892; https://doi.org/10.3390/cells14120892 - 13 Jun 2025
Abstract
Recent studies on myogenic satellite cells (SCs) in Duchenne muscular dystrophy (DMD) documented altered division capacities and impaired regeneration potential of SCs in DMD patients and animal models. It remains unknown, however, if SC-intrinsic effects trigger these deficiencies at pre-contractile stages of myogenesis [...] Read more.
Recent studies on myogenic satellite cells (SCs) in Duchenne muscular dystrophy (DMD) documented altered division capacities and impaired regeneration potential of SCs in DMD patients and animal models. It remains unknown, however, if SC-intrinsic effects trigger these deficiencies at pre-contractile stages of myogenesis rather than resulting from the pathologic environment. In this study, we isolated SCs from a porcine DMD model and age-matched wild-type (WT) piglets for comprehensive analysis. Using immunofluorescence, differentiation assays, traction force microscopy (TFM), RNA-seq, and label-free proteomic measurements, SCs behavior was characterized, and molecular changes were investigated. TFM revealed significantly higher average traction forces in DMD than WT SCs (90.4 ± 10.5 Pa vs. 66.9 ± 8.9 Pa; p = 0.0018). We identified 1390 differentially expressed genes and 1261 proteins with altered abundance in DMD vs. WT SCs. Dysregulated pathways uncovered by gene ontology (GO) enrichment analysis included sarcomere organization, focal adhesion, and response to hypoxia. Multi-omics factor analysis (MOFA) integrating transcriptomic and proteomic data, identified five factors accounting for the observed variance with an overall higher contribution of the transcriptomic data. Our findings suggest that SC impairments result from their inherent genetic abnormality rather than from environmental influences. The observed biological changes are intrinsic and not reactive to the pathological surrounding of DMD muscle. Full article
(This article belongs to the Special Issue Skeletal Muscle: Structure, Physiology and Diseases)
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