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Biomolecules
Special Issues
Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies
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Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 9871

Special Issue Editors

Dr. Tatiana L. Nemirovskaya

E-Mail Website
Guest Editor
Institute for Biomedical Problems, Russian Academy of Sciences, Moscow 123007, Russia
Interests: p38α-MAPK signaling; skeletal muscle
Dr. Tatiana Kostrominova

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, Indiana University School of Medicine-Northwest, 3400 Broadway St., Gary, IN 46408-1197, USA
Interests: skeletal muscle; tendon; aging; muscle denervation; muscle unloading; obesity; myokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle is essential for locomotion, maintaining posture, respiration (diaphragm), and phonation (laryngeal muscles). In addition, skeletal muscle plays a critical role in the whole-body metabolism. Skeletal muscle atrophy caused by a variety of conditions severely impairs muscle function. Skeletal muscle hypertrophy is adaptation to exercise and some other physiological processes. Muscle hypertrophy can improve muscle structure and function. Despite numerous published studies, the mechanisms regulating skeletal muscle atrophy and hypertrophy are still not completely understood.

In this Special Issue, we invite manuscripts on recent advances in the understanding of processes regulating skeletal muscle atrophy associated with diseases, aging, and unloading and muscle hypertrophy in response to exercise and other physiological adaptations.

A new Special Issue will be published in the Open Access journal Biomolecules (ISSN 2218-273X; 5-Year IF 6.19): “Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies”.

In this Special Issue, we invite authors to submit original research and review articles revealing mechanisms of skeletal muscle atrophy and hypertrophy, including but not limited to the following topics:

  • Signaling mechanisms involved in skeletal muscle atrophy and hypertrophy;
  • Mechanisms of unloading-induced changes in gene expression and signaling in skeletal muscle;
  • Denervation-induced skeletal muscle atrophy;
  • Aging-related skeletal muscle atrophy;
  • Skeletal muscle atrophy caused by diseases (diabetes, Duchenne atrophy, etc.);
  • Tenotomy-related skeletal muscle atrophy;
  • Exercise-induced muscle hypertrophy;
  • Hormones and growth factors-induced skeletal muscle atrophy and hypertrophy;
  • Role of satellite cells in muscle hypertrophy;
  • Regulatory mechanisms of muscle protein synthesis involved in atrophy and hypertrophy;
  • Therapies to counteract muscle atrophy.

Dr. Tatiana L. Nemirovskaya
Dr. Tatiana Kostrominova
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. Biomolecules 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
  • atrophy
  • unloading
  • denervation
  • aging
  • tenotomy
  • gene expression
  • signaling pathways

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Published Papers (3 papers)

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Research

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20 pages, 4700 KiB  
Article
The Effect of SERCA Activation on Functional Characteristics and Signaling of Rat Soleus Muscle upon 7 Days of Unloading
by Kristina A. Sharlo, Irina D. Lvova, Sergey A. Tyganov, Ksenia A. Zaripova, Svetlana P. Belova, Tatiana Y. Kostrominova, Boris S. Shenkman and Tatiana L. Nemirovskaya
Biomolecules 2023, 13(9), 1354; https://doi.org/10.3390/biom13091354 - 6 Sep 2023
Cited by 5 | Viewed by 1616
Abstract
Skeletal muscle abnormalities and atrophy during unloading are accompanied by the accumulation of excess calcium in the sarcoplasm. We hypothesized that calcium accumulation may occur, among other mechanisms, due to the inhibition of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) activity. Consequently, the use [...] Read more.
Skeletal muscle abnormalities and atrophy during unloading are accompanied by the accumulation of excess calcium in the sarcoplasm. We hypothesized that calcium accumulation may occur, among other mechanisms, due to the inhibition of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) activity. Consequently, the use of the SERCA activator will reduce the level of calcium in the sarcoplasm and prevent the negative consequences of muscle unloading. Wistar rats were randomly assigned into one of three groups (eight rats per group): control rats with placebo (C), 7 days of unloading/hindlimb suspension with placebo (7HS), and 7 days of unloading treated with SERCA activator CDN1163 (7HSC). After seven days of unloading the soleus muscle, the 7HS group displayed increased fatigue in the ex vivo test, a significant increase in the level of calcium-dependent CaMK II phosphorylation and the level of tropomyosin oxidation, as well as a decrease in the content of mitochondrial DNA and protein, slow-type myosin mRNA, and the percentage of slow-type muscle fibers. All of these changes were prevented in the 7HSC group. Moreover, treatment with CDN1163 blocked a decrease in the phosphorylation of p70S6k, an increase in eEF2 phosphorylation, and an increase in MuRF-1 mRNA expression. Nevertheless, there were no differences in the degree of fast and slow muscle fiber atrophy between the 7HS and 7HSC groups. Conclusion: SERCA activation during 7 days of unloading prevented an increase in soleus fatigue, the decrease of slow-type myosin, mitochondrial markers, and markers of calcium homeostasis but had no effect on muscle atrophy. Full article
(This article belongs to the Special Issue Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies)
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16 pages, 1215 KiB  
Article
Muscle-Specific Ablation of Glucose Transporter 1 (GLUT1) Does Not Impair Basal or Overload-Stimulated Skeletal Muscle Glucose Uptake
by Shawna L. McMillin, Parker L. Evans, William M. Taylor, Luke A. Weyrauch, Tyler J. Sermersheim, Steven S. Welc, Monique R. Heitmeier, Richard C. Hresko, Paul W. Hruz, Francoise Koumanov, Geoffrey D. Holman, E. Dale Abel and Carol A. Witczak
Biomolecules 2022, 12(12), 1734; https://doi.org/10.3390/biom12121734 - 23 Nov 2022
Cited by 3 | Viewed by 3558
Abstract
Glucose transporter 1 (GLUT1) is believed to solely mediate basal (insulin-independent) glucose uptake in skeletal muscle; yet recent work has demonstrated that mechanical overload, a model of resistance exercise training, increases muscle GLUT1 levels. The primary objective of this study was to determine [...] Read more.
Glucose transporter 1 (GLUT1) is believed to solely mediate basal (insulin-independent) glucose uptake in skeletal muscle; yet recent work has demonstrated that mechanical overload, a model of resistance exercise training, increases muscle GLUT1 levels. The primary objective of this study was to determine if GLUT1 is necessary for basal or overload-stimulated muscle glucose uptake. Muscle-specific GLUT1 knockout (mGLUT1KO) mice were generated and examined for changes in body weight, body composition, metabolism, systemic glucose regulation, muscle glucose transporters, and muscle [3H]-2-deoxyglucose uptake ± the GLUT1 inhibitor BAY-876. [3H]-hexose uptake ± BAY-876 was also examined in HEK293 cells-expressing GLUT1-6 or GLUT10. mGLUT1KO mice exhibited no impairments in body weight, lean mass, whole body metabolism, glucose tolerance, basal or overload-stimulated muscle glucose uptake. There was no compensation by the insulin-responsive GLUT4. In mGLUT1KO mouse muscles, overload stimulated higher expression of mechanosensitive GLUT6, but not GLUT3 or GLUT10. In control and mGLUT1KO mouse muscles, 0.05 µM BAY-876 impaired overload-stimulated, but not basal glucose uptake. In the GLUT-HEK293 cells, BAY-876 inhibited glucose uptake via GLUT1, GLUT3, GLUT4, GLUT6, and GLUT10. Collectively, these findings demonstrate that GLUT1 does not mediate basal muscle glucose uptake and suggest that a novel glucose transport mechanism mediates overload-stimulated glucose uptake. Full article
(This article belongs to the Special Issue Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies)
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Review

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26 pages, 1410 KiB  
Review
Muscle Involvement in Amyotrophic Lateral Sclerosis: Understanding the Pathogenesis and Advancing Therapeutics
by Elisa Duranti and Chiara Villa
Biomolecules 2023, 13(11), 1582; https://doi.org/10.3390/biom13111582 - 26 Oct 2023
Cited by 7 | Viewed by 3432
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal condition characterized by the selective loss of motor neurons in the motor cortex, brainstem, and spinal cord. Muscle involvement, muscle atrophy, and subsequent paralysis are among the main features of this disease, which is defined as [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a fatal condition characterized by the selective loss of motor neurons in the motor cortex, brainstem, and spinal cord. Muscle involvement, muscle atrophy, and subsequent paralysis are among the main features of this disease, which is defined as a neuromuscular disorder. ALS is a persistently progressive disease, and as motor neurons continue to degenerate, individuals with ALS experience a gradual decline in their ability to perform daily activities. Ultimately, muscle function loss may result in paralysis, presenting significant challenges in mobility, communication, and self-care. While the majority of ALS research has traditionally focused on pathogenic pathways in the central nervous system, there has been a great interest in muscle research. These studies were carried out on patients and animal models in order to better understand the molecular mechanisms involved and to develop therapies aimed at improving muscle function. This review summarizes the features of ALS and discusses the role of muscle, as well as examines recent studies in the development of treatments. Full article
(This article belongs to the Special Issue Muscle Atrophy and Hypertrophy: Mechanisms and Potential Therapies)
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