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Advances in Muscle Research in Health and Disease
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Advances in Muscle Research in Health and Disease

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

Deadline for manuscript submissions: 31 May 2024 | Viewed by 7740

Special Issue Editor

Prof. Dr. Wan Lee

E-Mail Website
Guest Editor
1. Department of Biochemistry, Dongguk University School of Medicine, Gyeongju 38066, Republic of Korea
2. Channelopathy Research Center (CRC), Dongguk University School of Medicine, Ilsan 10326, Republic of Korea
Interests: mechanotransduction; cytoskeleton remodeling; proliferation; differentiation; myogenesis; sarcopenia; insulin resistance; diabetes; metabolism; glucose metabolism; lipid metabolism; metabolic diseases; energy metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Muscles, consisting of skeletal, cardiac, and smooth muscle, comprise a significant portion of total body mass and are primarily essential for human vital functions. Muscle is also the largest depot for glucose disposal, amino acid storage, and coordination of whole-body metabolism via the consumption, distribution, and transportation of nutrients and other substrates. Muscle homeostasis is regulated by both endogenous and exogenous factors, which interact to influence both its structure and function. The advances in dietary, pharmacological, and therapeutic strategies to maintain muscle health, while stressing prevention and understanding of muscular system-related disorders, have highlighted the significance of muscle in recent decades. Furthermore, the recent rediscovery of muscle as endocrine organs has changed innovative notions in biomedicine by broadening the concept of systemic integration.

This Special Issue will explore new insights, aiming to present the most recent findings and advances in this field, outlining future prospects in all aspects of muscle research. We encourage original research articles as well as review articles on the structure, types, development, regeneration, functions, and roles of muscles, in addition to discussions of muscle-derived disorders that may affect human health.

Prof. Dr. Wan Lee
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. Cells is an international peer-reviewed open access semimonthly 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
  • cardiac muscle
  • smooth muscle
  • myocyte
  • vascular smooth muscle cell
  • stem cell
  • development
  • homeostasis
  • regeneration
  • biomarker
  • therapeutic target

Published Papers (5 papers)

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Research

15 pages, 3277 KiB  
Article
Lysine Distinctively Manipulates Myogenic Regulatory Factors and Wnt/Ca2+ Pathway in Slow and Fast Muscles, and Their Satellite Cells of Postnatal Piglets
by Xiaofan Wang, Xiaoyin Zong, Mao Ye, Chenglong Jin, Tao Xu, Jinzeng Yang, Chunqi Gao, Xiuqi Wang and Huichao Yan
Cells 2024, 13(7), 650; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13070650 - 08 Apr 2024
Viewed by 541
Abstract
Muscle regeneration, representing an essential homeostatic process, relies mainly on the myogenic progress of resident satellite cells, and it is modulated by multiple physical and nutritional factors. Here, we investigated how myogenic differentiation-related factors and pathways respond to the first limiting amino acid [...] Read more.
Muscle regeneration, representing an essential homeostatic process, relies mainly on the myogenic progress of resident satellite cells, and it is modulated by multiple physical and nutritional factors. Here, we investigated how myogenic differentiation-related factors and pathways respond to the first limiting amino acid lysine (Lys) in the fast and slow muscles, and their satellite cells (SCs), of swine. Thirty 28-day-old weaned piglets with similar body weights were subjected to three diet regimens: control group (d 0–28: 1.31% Lys, n = 12), Lys-deficient group (d 0–28: 0.83% Lys, n = 12), and Lys rescue group (d 0–14: 0.83% Lys; d 15–28: 1.31% Lys, n = 6). Pigs on d 15 and 29 were selectively slaughtered for muscular parameters evaluation. Satellite cells isolated from fast (semimembranosus) and slow (semitendinosus) muscles were also selected to investigate differentiation ability variations. We found Lys deficiency significantly hindered muscle development in both fast and slow muscles via the distinct manipulation of myogenic regulatory factors and the Wnt/Ca2+ pathway. In the SC model, Lys deficiency suppressed the Wnt/Ca2+ pathways and myosin heavy chain, myogenin, and myogenic regulatory factor 4 in slow muscle SCs but stimulated them in fast muscle SCs. When sufficient Lys was attained, the fast muscle-derived SCs Wnt/Ca2+ pathway (protein kinase C, calcineurin, calcium/calmodulin-dependent protein kinase II, and nuclear factor of activated T cells 1) was repressed, while the Wnt/Ca2+ pathway of its counterpart was stimulated to further the myogenic differentiation. Lys potentially manipulates the differentiation of porcine slow and fast muscle myofibers via the Wnt/Ca2+ pathway in opposite trends. Full article
(This article belongs to the Special Issue Advances in Muscle Research in Health and Disease)
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23 pages, 14499 KiB  
Article
Secretome from Magnetically Stimulated Muscle Exhibits Anticancer Potency: Novel Preconditioning Methodology Highlighting HTRA1 Action
by Yee Kit Tai, Jan Nikolas Iversen, Karen Ka Wing Chan, Charlene Hui Hua Fong, Rafhanah Banu Abdul Razar, Sharanya Ramanan, Lye Yee Jasmine Yap, Jocelyn Naixin Yin, Shi Jie Toh, Craig Jun Kit Wong, Pei Fern Angele Koh, Ruby Yun Ju Huang and Alfredo Franco-Obregón
Cells 2024, 13(5), 460; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13050460 - 05 Mar 2024
Viewed by 3275
Abstract
Briefly (10 min) exposing C2C12 myotubes to low amplitude (1.5 mT) pulsed electromagnetic fields (PEMFs) generated a conditioned media (pCM) that was capable of mitigating breast cancer cell growth, migration, and invasiveness in vitro, whereas the conditioned media harvested from unexposed myotubes, representing [...] Read more.
Briefly (10 min) exposing C2C12 myotubes to low amplitude (1.5 mT) pulsed electromagnetic fields (PEMFs) generated a conditioned media (pCM) that was capable of mitigating breast cancer cell growth, migration, and invasiveness in vitro, whereas the conditioned media harvested from unexposed myotubes, representing constitutively released secretome (cCM), was less effective. Administering pCM to breast cancer microtumors engrafted onto the chorioallantoic membrane of chicken eggs reduced tumor volume and vascularity. Blood serum collected from PEMF-exposed or exercised mice allayed breast cancer cell growth, migration, and invasiveness. A secretome preconditioning methodology is presented that accentuates the graded anticancer potencies of both the cCM and pCM harvested from myotubes, demonstrating an adaptive response to pCM administered during early myogenesis that emulated secretome-based exercise adaptations observed in vivo. HTRA1 was shown to be upregulated in pCM and was demonstrated to be necessary and sufficient for the anticancer potency of the pCM; recombinant HTRA1 added to basal media recapitulated the anticancer effects of pCM and antibody-based absorption of HTRA1 from pCM precluded its anticancer effects. Brief and non-invasive PEMF stimulation may represent a method to commandeer the secretome response of muscle, both in vitro and in vivo, for clinical exploitation in breast and other cancers. Full article
(This article belongs to the Special Issue Advances in Muscle Research in Health and Disease)
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17 pages, 3259 KiB  
Article
WAVE2 Is a Vital Regulator in Myogenic Differentiation of Progenitor Cells through the Mechanosensitive MRTFA–SRF Axis
by Mai Thi Nguyen, Quoc Kiet Ly, Hyun-Jung Kim and Wan Lee
Cells 2024, 13(1), 9; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13010009 - 20 Dec 2023
Viewed by 789
Abstract
Skeletal myogenesis is an intricate process involving the differentiation of progenitor cells into myofibers, which is regulated by actin cytoskeletal dynamics and myogenic transcription factors. Although recent studies have demonstrated the pivotal roles of actin-binding proteins (ABPs) as mechanosensors and signal transducers, the [...] Read more.
Skeletal myogenesis is an intricate process involving the differentiation of progenitor cells into myofibers, which is regulated by actin cytoskeletal dynamics and myogenic transcription factors. Although recent studies have demonstrated the pivotal roles of actin-binding proteins (ABPs) as mechanosensors and signal transducers, the biological significance of WAVE2 (Wiskott–Aldrich syndrome protein family member 2), an ABP essential for actin polymerization, in myogenic differentiation of progenitor cells has not been investigated. Our study provides important insights into the regulatory roles played by WAVE2 in the myocardin-related transcription factor A (MRTFA)–serum response factor (SRF) signaling axis and differentiation of myoblasts. We demonstrate that WAVE2 expression is induced during myogenic differentiation and plays a pivotal role in actin cytoskeletal remodeling in C2C12 myoblasts. Knockdown of WAVE2 in C2C12 cells reduced filamentous actin levels, increased globular actin accumulation, and impaired the nuclear translocation of MRTFA. Furthermore, WAVE2 depletion in myoblasts inhibited the expression and transcriptional activity of SRF and suppressed cell proliferation in myoblasts. Consequently, WAVE2 knockdown suppressed myogenic regulatory factors (i.e., MyoD, MyoG, and SMYD1) expressions, thereby hindering the differentiation of myoblasts. Thus, this study suggests that WAVE2 is essential for myogenic differentiation of progenitor cells by modulating the mechanosensitive MRTFA–SRF axis. Full article
(This article belongs to the Special Issue Advances in Muscle Research in Health and Disease)
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20 pages, 8243 KiB  
Article
Spatial Transcriptomics Reveals Signatures of Histopathological Changes in Muscular Sarcoidosis
by Hippolyte Lequain, Cyril Dégletagne, Nathalie Streichenberger, Julie Valantin, Thomas Simonet, Laurent Schaeffer, Pascal Sève and Pascal Leblanc
Cells 2023, 12(23), 2747; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12232747 - 30 Nov 2023
Viewed by 1317
Abstract
Sarcoidosis is a multisystemic disease characterized by non-caseating granuloma infiltrating various organs. The form with symptomatic muscular involvement is called muscular sarcoidosis. The impact of immune cells composing the granuloma on the skeletal muscle is misunderstood. Here, we investigated the granuloma–skeletal muscle interactions [...] Read more.
Sarcoidosis is a multisystemic disease characterized by non-caseating granuloma infiltrating various organs. The form with symptomatic muscular involvement is called muscular sarcoidosis. The impact of immune cells composing the granuloma on the skeletal muscle is misunderstood. Here, we investigated the granuloma–skeletal muscle interactions through spatial transcriptomics on two patients affected by muscular sarcoidosis. Five major transcriptomic clusters corresponding to perigranuloma, granuloma, and three successive muscle tissue areas (proximal, intermediate, and distal) around the granuloma were identified. Analyses revealed upregulated pathways in the granuloma corresponding to the activation of T-lymphocytes and monocytes/macrophages cytokines, the upregulation of extracellular matrix signatures, and the induction of the TGF-β signaling in the perigranuloma. A comparison between the proximal and distal muscles to the granuloma revealed an inverse correlation between the distance to the granuloma and the upregulation of cellular response to interferon-γ/α, TNF-α, IL-1,4,6, fibroblast proliferation, epithelial to mesenchymal cell transition, and the downregulation of muscle gene expression. These data shed light on the intercommunications between granulomas and the muscle tissue and provide pathophysiological mechanisms by showing that granuloma immune cells have a direct impact on proximal muscle tissue by promoting its progressive replacement by fibrosis via the expression of pro-inflammatory and profibrosing signatures. These data could possibly explain the evolution towards a state of disability for some patients. Full article
(This article belongs to the Special Issue Advances in Muscle Research in Health and Disease)
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23 pages, 6332 KiB  
Article
The Adiponectin Receptor Agonist, ALY688: A Promising Therapeutic for Fibrosis in the Dystrophic Muscle
by Nicolas Dubuisson, Romain Versele, Maria A. Davis-López de Carrizosa, Camille M. Selvais, Laurence Noel, Chloé Planchon, Peter Y. K. Van den Bergh, Sonia M. Brichard and Michel Abou-Samra
Cells 2023, 12(16), 2101; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12162101 - 19 Aug 2023
Cited by 1 | Viewed by 1310
Abstract
Duchenne muscular dystrophy (DMD) is one of the most devastating myopathies, where severe inflammation exacerbates disease progression. Previously, we demonstrated that adiponectin (ApN), a hormone with powerful pleiotropic effects, can efficiently improve the dystrophic phenotype. However, its practical therapeutic application is limited. In [...] Read more.
Duchenne muscular dystrophy (DMD) is one of the most devastating myopathies, where severe inflammation exacerbates disease progression. Previously, we demonstrated that adiponectin (ApN), a hormone with powerful pleiotropic effects, can efficiently improve the dystrophic phenotype. However, its practical therapeutic application is limited. In this study, we investigated ALY688, a small peptide ApN receptor agonist, as a potential novel treatment for DMD. Four-week-old mdx mice were subcutaneously treated for two months with ALY688 and then compared to untreated mdx and wild-type mice. In vivo and ex vivo tests were performed to assess muscle function and pathophysiology. Additionally, in vitro tests were conducted on human DMD myotubes. Our results showed that ALY688 significantly improved the physical performance of mice and exerted potent anti-inflammatory, anti-oxidative and anti-fibrotic actions on the dystrophic muscle. Additionally, ALY688 hampered myonecrosis, partly mediated by necroptosis, and enhanced the myogenic program. Some of these effects were also recapitulated in human DMD myotubes. ALY688’s protective and beneficial properties were mainly mediated by the AMPK-PGC-1α axis, which led to suppression of NF-κβ and TGF-β. Our results demonstrate that an ApN mimic may be a promising and effective therapeutic prospect for a better management of DMD. Full article
(This article belongs to the Special Issue Advances in Muscle Research in Health and Disease)
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