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Molecular Insight into Skeletal Muscle Atrophy and Regeneration
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Molecular Insight into Skeletal Muscle Atrophy and Regeneration

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: 20 December 2024 | Viewed by 6300

Special Issue Editors

Dr. Elena Nebot

E-Mail Website
Guest Editor
Department of Physiology, School of Medicine, Complutense University of Madrid, 28040 Madrid, Spain
Interests: nutrition; physical exercise; bone metabolism; musculoskeletal system
Dr. Teresa Priego Cuadra

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Nursing, Physiotherapy and Podiatry, Complutense University of Madrid, 28040 Madrid, Spain
Interests: muscular atrophy; IGF-1 system; inflammation; stress; metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Ana Isabel Martín Velasco

E-Mail Website
Guest Editor
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain
Interests: muscular atrophy; IGF-1 system; inflammation; stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle wasting can be induced by chronic illnesses, aging, malnutrition, disease, and acute/chronic inflammatory conditions. Muscle atrophy leads to mobility, fragility, and a loss of independence, while also increasing the mortality and morbidity of the illness.

Muscle regeneration occurs after muscle injury, exercise, or physiological demands. Muscle regeneration involves inflammation, activation, proliferation, differentiation, and the maturation of satellite cells. Growth factors and mechanical stress from exercise play critical roles in promoting this process.

Therefore, understanding the processes of skeletal muscle wasting and regeneration offers insights for developing therapies to mitigate muscle loss and promote muscle recovery.

This Special Issue invites both original articles and reviews that can provide the readers of IJMS with novel research on the molecular mechanisms and possible treatments related to enhancing muscle regeneration and counteracting muscle wasting, such as growth factors, gene therapy, stem cell transplantation, exercise, and nutraceutical interventions.

Dr. Elena Nebot
Dr. Teresa Priego Cuadra
Dr. Ana Isabel Martín Velasco
Guest Editors

Manuscript Submission Information

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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 atrophy
  • muscle regeneration
  • sarcopenia
  • cachexia
  • satellite cells
  • autophagy
  • proteolytic system
  • growth factors
  • myokines
  • physical exercise
  • nutrition
  • bone metabolism

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Published Papers (7 papers)

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Research

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32 pages, 15121 KiB  
Article
SMN Deficiency Induces an Early Non-Atrophic Myopathy with Alterations in the Contractile and Excitatory Coupling Machinery of Skeletal Myofibers in the SMN∆7 Mouse Model of Spinal Muscular Atrophy
by María T. Berciano, Alaó Gatius, Alba Puente-Bedia, Alexis Rufino-Gómez, Olga Tarabal, José C. Rodríguez-Rey, Jordi Calderó, Miguel Lafarga and Olga Tapia
Int. J. Mol. Sci. 2024, 25(22), 12415; https://doi.org/10.3390/ijms252212415 - 19 Nov 2024
Viewed by 324
Abstract
Spinal muscular atrophy (SMA) is caused by a deficiency of the ubiquitously expressed survival motor neuron (SMN) protein. The main pathological hallmark of SMA is the degeneration of lower motor neurons (MNs) with subsequent denervation and atrophy of skeletal muscle. However, increasing evidence [...] Read more.
Spinal muscular atrophy (SMA) is caused by a deficiency of the ubiquitously expressed survival motor neuron (SMN) protein. The main pathological hallmark of SMA is the degeneration of lower motor neurons (MNs) with subsequent denervation and atrophy of skeletal muscle. However, increasing evidence indicates that low SMN levels not only are detrimental to the central nervous system (CNS) but also directly affect other peripheral tissues and organs, including skeletal muscle. To better understand the potential primary impact of SMN deficiency in muscle, we explored the cellular, ultrastructural, and molecular basis of SMA myopathy in the SMNΔ7 mouse model of severe SMA at an early postnatal period (P0-7) prior to muscle denervation and MN loss (preneurodegenerative [PND] stage). This period contrasts with the neurodegenerative (ND) stage (P8-14), in which MN loss and muscle atrophy occur. At the PND stage, we found that SMN∆7 mice displayed early signs of motor dysfunction with overt myofiber alterations in the absence of atrophy. We provide essential new ultrastructural data on focal and segmental lesions in the myofibrillar contractile apparatus. These lesions were observed in association with specific myonuclear domains and included abnormal accumulations of actin-thin myofilaments, sarcomere disruption, and the formation of minisarcomeres. The sarcoplasmic reticulum and triads also exhibited ultrastructural alterations, suggesting decoupling during the excitation–contraction process. Finally, changes in intermyofibrillar mitochondrial organization and dynamics, indicative of mitochondrial biogenesis overactivation, were also found. Overall, our results demonstrated that SMN deficiency induces early and MN loss-independent alterations in myofibers that essentially contribute to SMA myopathy. This strongly supports the growing body of evidence indicating the existence of intrinsic alterations in the skeletal muscle in SMA and further reinforces the relevance of this peripheral tissue as a key therapeutic target for the disease. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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16 pages, 4776 KiB  
Article
USP2 Mitigates Reactive Oxygen Species-Induced Mitochondrial Damage via UCP2 Expression in Myoblasts
by Hiroshi Kitamura, Masaki Fujimoto, Mayuko Hashimoto, Hironobu Yasui and Osamu Inanami
Int. J. Mol. Sci. 2024, 25(22), 11936; https://doi.org/10.3390/ijms252211936 - 6 Nov 2024
Viewed by 380
Abstract
Ubiquitin-specific protease 2 (USP2) maintains mitochondrial integrity in culture myoblasts. In this study, we investigated the molecular mechanisms underlying the protective role of USP2 in mitochondria. The knockout (KO) of the Usp2 gene or the chemical inhibition of USP2 induced a robust accumulation [...] Read more.
Ubiquitin-specific protease 2 (USP2) maintains mitochondrial integrity in culture myoblasts. In this study, we investigated the molecular mechanisms underlying the protective role of USP2 in mitochondria. The knockout (KO) of the Usp2 gene or the chemical inhibition of USP2 induced a robust accumulation of mitochondrial reactive oxygen species (ROS), accompanied by defects in mitochondrial membrane potential, in C2C12 myoblasts. ROS removal by N-acetyl-L-cysteine restored the mitochondrial dysfunction induced by USP2 deficiency. Comprehensive RT-qPCR screening and following protein analysis indicated that both the genetic and chemical inhibition of USP2 elicited a decrease in uncoupling protein 2 (UCP2) at mRNA and protein levels. Accordingly, the introduction of a Ucp2-expressing construct effectively recovered the mitochondrial membrane potential, entailing an increment in the intracellular ATP level in Usp2KO C2C12 cells. In contrast, USP2 deficiency also decreased peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) protein in C2C12 cells, while it upregulated Ppargc1a mRNA. Overexpression studies indicated that USP2 potentially stabilizes PGC1α in an isopeptidase-dependent manner. Given that PGC1α is an inducer of UCP2 in C2C12 cells, USP2 might ameliorate mitochondrial ROS by maintaining the PGC1α–UCP2 axis in myoblasts. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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16 pages, 3395 KiB  
Article
An Amino Acid Mixture to Counteract Skeletal Muscle Atrophy: Impact on Mitochondrial Bioenergetics
by Francesco Bellanti, Aurelio Lo Buglio, Giuseppe Pannone, Maria Carmela Pedicillo, Ilenia Sara De Stefano, Angela Pignataro, Cristiano Capurso and Gianluigi Vendemiale
Int. J. Mol. Sci. 2024, 25(11), 6056; https://doi.org/10.3390/ijms25116056 - 31 May 2024
Viewed by 794
Abstract
Skeletal muscle atrophy (SMA) is caused by a rise in muscle breakdown and a decline in protein synthesis, with a consequent loss of mass and function. This study characterized the effect of an amino acid mixture (AA) in models of SMA, focusing on [...] Read more.
Skeletal muscle atrophy (SMA) is caused by a rise in muscle breakdown and a decline in protein synthesis, with a consequent loss of mass and function. This study characterized the effect of an amino acid mixture (AA) in models of SMA, focusing on mitochondria. C57/Bl6 mice underwent immobilization of one hindlimb (I) or cardiotoxin-induced muscle injury (C) and were compared with controls (CTRL). Mice were then administered AA in drinking water for 10 days and compared to a placebo group. With respect to CTRL, I and C reduced running time and distance, along with grip strength; however, the reduction was prevented by AA. Tibialis anterior (TA) muscles were used for histology and mitochondria isolation. I and C resulted in TA atrophy, characterized by a reduction in both wet weight and TA/body weight ratio and smaller myofibers than those of CTRL. Interestingly, these alterations were lightly observed in mice treated with AA. The mitochondrial yield from the TA of I and C mice was lower than that of CTRL but not in AA-treated mice. AA also preserved mitochondrial bioenergetics in TA muscle from I and C mice. To conclude, this study demonstrates that AA prevents loss of muscle mass and function in SMA by protecting mitochondria. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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22 pages, 9950 KiB  
Article
Transcriptome and Metabolome Profiling Provide New Insights into Disuse Muscle Atrophy in Chicken: The Potential Role of Fast-Twitch Muscle Fibers
by Zipei Yao, Lijin Guo, Li Zhang and Qinghua Nie
Int. J. Mol. Sci. 2024, 25(6), 3516; https://doi.org/10.3390/ijms25063516 - 20 Mar 2024
Viewed by 1559
Abstract
Disuse muscle atrophy is a disease caused by restricted activity, affecting human health and animal protein quality. While extensive research on its mechanism has been studied in mammals, comparatively little is known about this process in chickens, which are a significant source of [...] Read more.
Disuse muscle atrophy is a disease caused by restricted activity, affecting human health and animal protein quality. While extensive research on its mechanism has been studied in mammals, comparatively little is known about this process in chickens, which are a significant source of protein for human consumption worldwide. Understanding the mechanisms underlying skeletal muscle atrophy in chickens is crucial for improving poultry health and productivity, as well as for developing strategies to mitigate muscle loss. In this study, two groups of chickens were subjected to limb immobilization for two and four weeks, respectively, in order to induce disuse muscle atrophy and uniformly sampled gastrocnemius muscle at the fourth week. A combined analysis of the transcriptome and metabolome was conducted to investigate the mechanisms of disuse-induced muscle atrophy. Through H&E staining and immunofluorescence, we found that, compared to slow-twitch muscle fibers, the fast-twitch muscle fibers showed a greater reduction in cross-sectional area in the immobilized leg, and were also the main driver of changes in cross-sectional area observed in the non-immobilized leg. Integrated analysis revealed that differentially expressed genes (DEGs) and differentially accumulated metabolites (DAMs) were mainly enriched in pathways related to energy metabolism, such as fatty acid metabolism, oxidative phosphorylation (OXPHOS), and glycolysis. These results provide important insights for further research on disuse muscle atrophy. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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14 pages, 1662 KiB  
Article
Time-Dependent Changes in Muscle IGF1-IGFBP5-PAPP System after Sciatic Denervation
by Ana Isabel Martín, Álvaro Moreno-Rupérez, Elena Nebot, Miriam Granado, Daniel Jaque, M. Paz Nieto-Bona, Asunción López-Calderón and Teresa Priego
Int. J. Mol. Sci. 2023, 24(18), 14112; https://doi.org/10.3390/ijms241814112 - 14 Sep 2023
Viewed by 1572
Abstract
Denervation-induced muscle atrophy is a frequent cause of skeletal muscle diseases. However, the role of the most important muscle growth factor, insulin-like growth factor (IGF-1), in this process is poorly understood. IGF-1 activity is controlled by six IGF-1 binding proteins (IGFBPs). In skeletal [...] Read more.
Denervation-induced muscle atrophy is a frequent cause of skeletal muscle diseases. However, the role of the most important muscle growth factor, insulin-like growth factor (IGF-1), in this process is poorly understood. IGF-1 activity is controlled by six IGF-1 binding proteins (IGFBPs). In skeletal muscle, IGFBP-5 seems to have an important role in atrophic processes. Furthermore, pappalysins (PAPP-A) modulate muscle growth by increasing IGF-1 bioavailability through IGFBP cleavage. We aimed to study the time-dependent changes in the IGF1-IGFBP5-PAPP system and its regulators in gastrocnemius muscle after sciatic denervation. Gastrocnemius atrophy and overexpression of IGF-1 was observed from day 3 post-denervation. The proteolytic factors measured were elevated from day 1 post-denervation onwards. Expression of both IGFBP-5 and pappalysins were increased on days 1 and 3. Subsequently, on days 7 to 14 pappalysins returned to control levels while IGFBP-5 remained elevated. The ratio IGFBP-5/PAPP-A was correlated with the main proteolytic markers. All data suggest that the initial increase of pappalysins could facilitate the IGF-1 action on muscle growth, whereas their subsequent decrease could lead to further muscle wasting. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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Review

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12 pages, 2319 KiB  
Review
Continuous Use During Disuse: Mechanisms and Effects of Spontaneous Activity of Unloaded Postural Muscle
by Boris S. Shenkman, Vitaliy E. Kalashnikov, Kristina A. Sharlo, Olga V. Turtikova, Roman O. Bokov and Timur M. Mirzoev
Int. J. Mol. Sci. 2024, 25(22), 12462; https://doi.org/10.3390/ijms252212462 - 20 Nov 2024
Viewed by 244
Abstract
In most mammals, postural soleus muscles are involved in the maintenance of the stability of the body in the gravitational field of Earth. It is well established that immediately after a laboratory rat is exposed to conditions of weightlessness (parabolic flight) or simulated [...] Read more.
In most mammals, postural soleus muscles are involved in the maintenance of the stability of the body in the gravitational field of Earth. It is well established that immediately after a laboratory rat is exposed to conditions of weightlessness (parabolic flight) or simulated microgravity (hindlimb suspension/unloading), a sharp decrease in soleus muscle electrical activity occurs. However, starting from the 3rd day of mechanical unloading, soleus muscle electrical activity begins to increase and reaches baseline levels approximately by the 14th day of hindlimb suspension. This phenomenon, observed in the course of rat hindlimb suspension, was named the “spontaneous electrical activity of postural muscle”. The present review discusses spinal mechanisms underlying the development of such spontaneous activity of rat soleus muscle and the effect of this activity on intracellular signaling in rat soleus muscle during mechanical unloading. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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13 pages, 988 KiB  
Review
Various Strategies of Tendon Stem/Progenitor Cell Reprogramming for Tendon Regeneration
by Sung Yong Ahn
Int. J. Mol. Sci. 2024, 25(21), 11745; https://doi.org/10.3390/ijms252111745 - 1 Nov 2024
Viewed by 552
Abstract
Rotator cuff tears (RCT) are the most common cause of shoulder pain among adults. “Rotator cuff” refers to the four muscles that cover the shoulder joint: supraspinatus, infraspinatus, subscapularis, and teres minor. These muscles help maintain the rotational movement and stability of the [...] Read more.
Rotator cuff tears (RCT) are the most common cause of shoulder pain among adults. “Rotator cuff” refers to the four muscles that cover the shoulder joint: supraspinatus, infraspinatus, subscapularis, and teres minor. These muscles help maintain the rotational movement and stability of the shoulder joint. RCT is a condition in which one or more of these four muscles become ruptured or damaged, causing pain in the arms and shoulders. RCT results from degenerative changes caused by chronic inflammation of the tendons and consequent tendon tissue defects. This phenomenon occurs because of the exhaustion of endogenous tendon stem cells. Tendon regeneration requires rejuvenation of these endogenous tendon stem/progenitor cells (TSPCs) prior to their growth phase. TSPCs exhibit clonogenicity, multipotency, and self-renewal properties; they express classical stem cell markers and genes associated with the tendon lineage. However, specific markers for TSPC are yet to be identified. In this review, we introduce novel TSPC markers and discuss various strategies for TSPC reprogramming. With further research, TSPC reprogramming technology could be adapted to treat age-related degenerative diseases, providing a new strategy for regenerative medicine. Full article
(This article belongs to the Special Issue Molecular Insight into Skeletal Muscle Atrophy and Regeneration)
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