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Biology
Special Issues
Repair and Regeneration of Skeletal Muscle
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Repair and Regeneration of Skeletal Muscle

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Developmental and Reproductive Biology".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 2951

Special Issue Editor

Prof. Dr. Huili Tong

E-Mail Website
Guest Editor
1. Key Laboratory of Animal Cellular and Genetics Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin 150030, China
2. Laboratory of Cell and Developmental Biology, Northeast Agricultural University, Harbin 150030, China
Interests: muscle post-injury regeneration and repair; muscle nutrition and disease

Special Issue Information

Dear Colleagues,

Skeletal muscle, as one of the most important organs in the human body, plays a variety of important physiological functions in human beings, such as movement and metabolism. Aging, chronic diseases, drug stimulation, physical trauma, and other factors usually cause skeletal muscle sarcopenia, atrophy, or injury. Severe skeletal muscle damage often impairs the function of skeletal-muscle-specific stem cells, muscle satellite cells (MuSCs), making it difficult to repair skeletal muscle injury and seriously affecting normal physiological activities and quality of life. This has always been a hot topic in the fields of life science and regenerative medicine. Therefore, this Special Issue welcomes submissions of research conducted from a wide range of angles, from studies elucidating the roles and developmental mechanisms of MuSCs to those exploring novel methods and strategies such as drug intervention, stem cell therapy, tissue engineering technology, and so on, for effectively promoting skeletal muscle regeneration and repair. We hope that our research will help to promote the regeneration and repair of skeletal muscle injury, maintain the homeostasis of skeletal muscle tissue, and restore the health of skeletal muscle.

Prof. Dr. Huili Tong
Guest Editor

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. Biology 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

  • skeletal muscle
  • sarcopenia
  • atrophy
  • muscle satellite cells
  • regeneration and repair

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Published Papers (2 papers)

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Research

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16 pages, 4478 KiB  
Article
PEAR1 Promotes Myoblast Proliferation Through Notch Signaling Pathway
by Yahao Zhao, Lu Zhang, Ruotong Hao, Shuang Li, Shufeng Li, Shuai Shi, Huili Tong and Bingchen Liu
Biology 2024, 13(12), 1063; https://doi.org/10.3390/biology13121063 - 19 Dec 2024
Viewed by 200
Abstract
PEAR1, also known as platelet endothelial aggregation receptor 1, is known to play a crucial role in the migration and differentiation of muscle satellite cells (MuSCs). However, its specific effects on skeletal muscle development and regeneration require further exploration. In this study, the [...] Read more.
PEAR1, also known as platelet endothelial aggregation receptor 1, is known to play a crucial role in the migration and differentiation of muscle satellite cells (MuSCs). However, its specific effects on skeletal muscle development and regeneration require further exploration. In this study, the expression of PEAR1; the proliferation marker proteins of Pax7, CCNB1, and PCNA; and the key molecules of N1-ICD, N2-ICD, and Hes1 were all increased gradually during the process of C2C12 cell proliferation. Furthermore, Western blotting and EdU results showed that when PEAR1 was over-expressed or inhibited, the proliferation status of C2C12 cell was increased or reduced respectively. This implied that PEAR1 could regulate myoblast proliferation and might be relate to Notch cell signaling pathway. A subsequent immunoprecipitation experiment result showed that the interaction between PEAR1 and Notch1 or Notch2, respectively. Then Western blotting and EdU results showed that the proliferation of C2C12 cell was inhibited under the treatment of Notch signaling pathway inhibitor RIN1. Meanwhile, the proliferation capacity of C2C12 cell could not be improved by treatment with RIN1 even though PEAR1 was over-expressed. These results showed that PEAR1 may regulated C2C12 cell proliferation though Notch signaling pathway. Additionally, a mouse model of muscle injury repair injected with bupivacaine hydrochloride was established in this study. Immunohistochemistry results exhibited that PEAR1 may regulate skeletal muscle post-injury regeneration relevant to Notch1 and Notch2 in different patterns. These findings provide valuable insights into the potential involvement of PEAR1 in skeletal muscle development and post-injury regeneration. Full article
(This article belongs to the Special Issue Repair and Regeneration of Skeletal Muscle)
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Review

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26 pages, 1328 KiB  
Review
From Brain to Muscle: The Role of Muscle Tissue in Neurodegenerative Disorders
by Elisa Duranti and Chiara Villa
Biology 2024, 13(9), 719; https://doi.org/10.3390/biology13090719 - 12 Sep 2024
Viewed by 2287
Abstract
Neurodegenerative diseases (NDs), like amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD), primarily affect the central nervous system, leading to progressive neuronal loss and motor and cognitive dysfunction. However, recent studies have revealed that muscle tissue also plays a significant [...] Read more.
Neurodegenerative diseases (NDs), like amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD), primarily affect the central nervous system, leading to progressive neuronal loss and motor and cognitive dysfunction. However, recent studies have revealed that muscle tissue also plays a significant role in these diseases. ALS is characterized by severe muscle wasting as a result of motor neuron degeneration, as well as alterations in gene expression, protein aggregation, and oxidative stress. Muscle atrophy and mitochondrial dysfunction are also observed in AD, which may exacerbate cognitive decline due to systemic metabolic dysregulation. PD patients exhibit muscle fiber atrophy, altered muscle composition, and α-synuclein aggregation within muscle cells, contributing to motor symptoms and disease progression. Systemic inflammation and impaired protein degradation pathways are common among these disorders, highlighting muscle tissue as a key player in disease progression. Understanding these muscle-related changes offers potential therapeutic avenues, such as targeting mitochondrial function, reducing inflammation, and promoting muscle regeneration with exercise and pharmacological interventions. This review emphasizes the importance of considering an integrative approach to neurodegenerative disease research, considering both central and peripheral pathological mechanisms, in order to develop more effective treatments and improve patient outcomes. Full article
(This article belongs to the Special Issue Repair and Regeneration of Skeletal Muscle)
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