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Molecular Insights on Myogenic Progenitors: Regulation of Differentiation

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: 30 September 2025 | Viewed by 505

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Guest Editor
Department of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ, USA
Interests: transcriptional regulation; biochemistry; chromatin; cell biology; DNA binding; Lamins
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Special Issue Information

Dear Colleagues,

Myogenic progenitors are essential for skeletal muscle development, regeneration, and repair. This series explores the molecular mechanisms governing their decision to renew and propagate or to differentiate, focusing on transcriptional and epigenetic regulation, cell signaling, mechanotransduction, and their interactions with the niche. By highlighting recent advances in myogenic progenitor biology, we aim to provide new insights into muscle regeneration, disease, and development of therapeutic strategies. This series will bring together innovative research to advance our understanding of myogenesis and its implications in health and disease. We invite contributions that expand our understanding of the molecular mechanisms of myogenic progenitor regulation and differentiation and their therapeutic implications.

Dr. James M. Holaska
Guest Editor

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Keywords

  • myogenic progenitors
  • skeletal muscle
  • muscle regeneration
  • myogenesis

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Published Papers (1 paper)

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16 pages, 4500 KB  
Article
Development of Emerin mRNA Lipid Nanoparticles to Rescue Myogenic Differentiation
by Nicholas Marano, Liza Elif Guner, Rachel S. Riley and James M. Holaska
Int. J. Mol. Sci. 2025, 26(16), 7774; https://doi.org/10.3390/ijms26167774 - 12 Aug 2025
Viewed by 365
Abstract
Emery–Dreifuss muscular dystrophy 1 (EDMD1) arises from mutations in EMD. Most EDMD1 patients lack detectable emerin expression. They experience symptoms such as skeletal muscle wasting, joint contractures, and cardiac conduction defects. Currently, physicians rely on treating patient symptoms without addressing the underlying [...] Read more.
Emery–Dreifuss muscular dystrophy 1 (EDMD1) arises from mutations in EMD. Most EDMD1 patients lack detectable emerin expression. They experience symptoms such as skeletal muscle wasting, joint contractures, and cardiac conduction defects. Currently, physicians rely on treating patient symptoms without addressing the underlying cause—lack of functional emerin protein. Thus, there is a need for therapeutic approaches that restore emerin protein expression to improve patient outcomes. One way would be to deliver emerin mRNA or protein directly to affected tissues to restore tissue homeostasis. Here, we evaluated the utility of lipid nanoparticles (LNPs) to deliver emerin mRNA to diseased cells. LNPs have been studied for decades and have recently been used clinically for vaccination and treatment of a myriad of diseases. Here, we show that the treatment of emerin-null myogenic progenitors with LNPs encapsulating emerin mRNA causes robust emerin protein expression that persists for at least 4 days. The treatment of differentiating emerin-null myogenic progenitors with 2.5 pg/cell emerin LNPs significantly improved their differentiation. The toxicity profiling of emerin mRNA LNP (EMD-LNP) dosing shows little toxicity at the effective dose. These data support the potential use of EMD-LNPs as a viable treatment option and establishes its utility for studying EDMD pathology. Full article
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