Gene and Cellular Signaling Related to Muscle

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 1316

Special Issue Editor


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Guest Editor

Special Issue Information

Dear Colleagues,

Skeletal muscle is incredibly adaptable, undergoing significant biochemical and structural changes in response to changes in activity levels, developmental cues, and environmental conditions. These changes are driven by complex alterations in gene expression that regulate muscle growth, differentiation, and function. Recent advances in molecular biology have provided insights into the intricate signaling pathways and regulatory networks that control these processes, offering a new understanding of skeletal muscle physiology and pathology. The molecular mechanisms underlying muscle atrophy and hypertrophy have been the focus of intensive research for several decades. Key signaling pathways, including those mediated by insulin-like growth factors (IGFs), myostatin, and various cytokines, have been identified as critical regulators of muscle mass. The role of transcription factors such as MyoD, myogenin, and FoxO in modulating gene expression during muscle growth and atrophy has also been well established. Despite this progress, our understanding of the full spectrum of molecular events driving muscle adaptation remains incomplete.

Emerging research highlights the significance of additional regulatory elements, including microRNAs, long non-coding RNAs, and epigenetic modifications, in controlling muscle gene expression. Moreover, the interplay between metabolic status, hormonal signals, and muscle cell signaling pathways underscores the complexity of muscle biology. Understanding these interactions is crucial for developing therapeutic strategies to combat muscle-wasting conditions associated with aging, chronic diseases, and metabolic disorders.

This Special Issue aims to combine original research articles and comprehensive reviews exploring the diverse cellular signaling pathways and genetic programs governing skeletal muscle function in health and disease.

We welcome contributions that address the following:

  • Molecular mechanisms of muscle growth, differentiation, and regeneration;
  • Pathways involved in muscle atrophy and hypertrophy;
  • Role of transcription factors and non-coding RNAs in muscle gene regulation;
  • Integration of metabolic signals and muscle cell signaling;
  • Muscle–bone interactions and their impact on musculoskeletal health;
  • Novel therapeutic targets for muscle-wasting diseases;
  • Advances in muscle tissue engineering and regenerative medicine

Dr. Khurshid Ahmad
Guest Editor

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Keywords

  • skeletal muscle
  • molecular mechanism
  • muscle atrophy
  • therapeutics
  • metabolic signals
  • satellite cells

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Published Papers (1 paper)

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Research

14 pages, 2457 KiB  
Article
Atrophic C2C12 Myotubes Activate Inflammatory Response of Macrophages In Vitro
by Cong Wu, Yishan Tong, Jiapeng Huang, Shuo Wang, Haruki Kobori, Ziwei Zhang and Katsuhiko Suzuki
Cells 2025, 14(5), 317; https://doi.org/10.3390/cells14050317 - 20 Feb 2025
Viewed by 868
Abstract
Background: Skeletal muscle wasting is commonly observed in aging, immobility, and chronic diseases. In pathological conditions, the impairment of skeletal muscle and immune system often occurs simultaneously. Recent studies have highlighted the initiative role of skeletal muscle in interactions with immune cells. However, [...] Read more.
Background: Skeletal muscle wasting is commonly observed in aging, immobility, and chronic diseases. In pathological conditions, the impairment of skeletal muscle and immune system often occurs simultaneously. Recent studies have highlighted the initiative role of skeletal muscle in interactions with immune cells. However, the impact of skeletal muscle wasting on macrophage inflammatory responses remains poorly understood. Methods: To investigate the effect of atrophic myotubes on the inflammatory response of macrophages, we established two in vitro models to induce myotube atrophy: one induced by D-galactose and the other by starvation. Conditioned medium (CM) from normal and atrophic myotubes were collected and administered to bone marrow-derived macrophages (BMDMs) from mice. Subsequently, lipopolysaccharide (LPS) stimulation was applied, and the expression of inflammatory cytokines was measured via RT-qPCR. Results: Both D-galactose and starvation treatments reduced myotube diameter and upregulated muscle atrophy-related gene expression. CM from both atrophic myotubes models augmented the gene expression of pro-inflammatory factors in BMDMs following LPS stimulation, including Il6, Il1b, and Nfkb1. Notably, CM from starvation-induced atrophic myotubes also enhanced Il12b, Tnf, and Nos2 expression in BMDMs after stimulation, a response not observed in D-galactose-induced atrophic myotubes. Conclusions: These findings suggest that CM from atrophic myotubes enhanced the expression of LPS-induced pro-inflammatory mediators in macrophages. Full article
(This article belongs to the Special Issue Gene and Cellular Signaling Related to Muscle)
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