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Skeletal Muscle Wasting, Regeneration, and Stem Cells

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: closed (31 July 2023) | Viewed by 2320

Special Issue Editors


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Guest Editor
Sezione di Istologia ed Embriologia, Dipartimento di Scienze della Vita e Sanità Pubblica, Fondazione Policlinico Universitario A. Gemelli IRCCS, 00168 Roma, Italy
Interests: molecular mechanisms involved in the regulation of regeneration, differentiation, and hypertrophy/atrophy of skeletal muscle in normal and pathological conditions
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Guest Editor
Department of Anatomy, Histology, Forensic Medicine and Orthopedics, Sapienza University of Rome, 00161 Roma, Italy
Interests: molecular mechanisms of skeletal muscle atrophy induced by physio/pathological defects in muscle and nerve interplay
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are serving as Guest Editors for the Special Issue “Skeletal Muscle Wasting, Regeneration and Stem Cells” for the journal International Journal of Molecular Sciences (ISSN 1422-0067). We hope that you are willing to participate given your expertise in this area and our confidence in the quality of your contributions.

Skeletal muscle wasting occurs during aging or pathological conditions, and it is characterized by a significant reduction in muscle mass and strength, lowering a patient’s quality of life and increasing morbidity and mortality. Muscle wasting involves an imbalance between protein synthesis and degradation, and it is the result of multifactorial processes such as chronic inflammation, increased levels of oxidative stress, mitochondrial dysfunctions, and impairment of the regenerative process.

The regenerative process is characterized by a coordinated sequence of events, resembling the embryonic development of skeletal muscle, and depends on the sequential expression of myogenic regulatory factors (MRFs) which act in cooperation with specific transcription factors, such as Pax7 and MEF2, to maintain and preserve tissue structure and functionality upon damaged stimuli. However, during aging or pathological conditions, this regenerative program is severely compromised, with a progressive loss of muscle mass and function. This effect seems to be closely related to the progressive loss of stem cell populations or the lack of signals that prevent damaged tissues from carrying out an efficient regeneration program.

The most useful strategies to counteract skeletal muscle wasting include physical exercise and nutritional supplementation; however, to date, no effective countermeasure for skeletal muscle atrophy has been developed.

This Special Issue calls for original articles and reviews that provide IJMS readers with the latest information on the molecular mechanisms involved in muscle wasting and regeneration and the role that stem cells play in these processes. Furthermore, particular attention will be paid to possible therapeutic strategies that aim to maintain skeletal muscle homeostasis.

Dr. Bianca Maria Scicchitano
Dr. Gabriella Dobrowolny
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.

Keywords

  • muscle wasting
  • oxidative stress
  • inflammation
  • nutrition
  • exercise
  • neuromuscular diseases
  • mitochondrial dysfunction
  • myopathy

Published Papers (1 paper)

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Research

18 pages, 17186 KiB  
Article
CircTCF4 Suppresses Proliferation and Differentiation of Goat Skeletal Muscle Satellite Cells Independent from AGO2 Binding
by Shuailong Zheng, Li Li, Helin Zhou, Xujia Zhang, Xiaoli Xu, Dinghui Dai, Siyuan Zhan, Jiaxue Cao, Jiazhong Guo, Tao Zhong, Linjie Wang and Hongping Zhang
Int. J. Mol. Sci. 2022, 23(21), 12868; https://doi.org/10.3390/ijms232112868 - 25 Oct 2022
Cited by 6 | Viewed by 1744
Abstract
The proliferation and differentiation of mammalian skeletal muscle satellite cells (MuSCs) are highly complicated. Apart from the regulatory signaling cascade driven by the protein-coding genes, non-coding RNAs such as microRNAs (miRNA) and circular RNAs (circRNAs) play essential roles in this biological process. However, [...] Read more.
The proliferation and differentiation of mammalian skeletal muscle satellite cells (MuSCs) are highly complicated. Apart from the regulatory signaling cascade driven by the protein-coding genes, non-coding RNAs such as microRNAs (miRNA) and circular RNAs (circRNAs) play essential roles in this biological process. However, circRNA functions in MuSCs proliferation and differentiation remain largely to be elucidated. Here, we screened for an exonic circTCF4 based on our previous RNA-Seq data, specifically expressed during the development of the longest dorsal muscle in goats. Subsequently, the circular structure and whole sequence of circTCF4 were verified using Sanger sequencing. Besides, circTCF4 was spatiotemporally expressed in multiple tissues from goats but strikingly enriched in muscles. Furthermore, circTCF4 suppressed MuSCs proliferation and differentiation, independent of AGO2 binding. Finally, we conducted Poly(A) RNA-Seq using cells treated with small interfering RNA targeting circTCF4 and found that circTCF4 would affect multiple signaling pathways, including the insulin signaling pathway and AMPK signaling pathway related to muscle differentiation. Our results provide additional solid evidence for circRNA regulating skeletal muscle formation. Full article
(This article belongs to the Special Issue Skeletal Muscle Wasting, Regeneration, and Stem Cells)
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