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Muscle Atrophy: From Bench to Bedside 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 4744

Special Issue Editor


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Guest Editor
INRAE, Unité de Nutrition Humaine, Université Clermont Auvergne, UMR 1019, F-63000 Clermont-Ferrand, France
Interests: skeletal muscle atrophy; ubiquitin proteasome system; E3 ligases; E2 ubiquitin conjugating enzymes
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Special Issue Information

Dear Colleagues,

The loss of muscle mass is a common adaptation to some physiological situations (e.g., bed rest), but also to many diseases (e.g., diabetes, cancer, heart failure, respiratory failure, renal failure, and sepsis), and is caused by an imbalance of both protein synthesis and protein degradation. Muscle loss contributes to frailty syndrome and is associated with an impaired quality of life and an increased risk of death, regardless of the causal disease. In addition, muscle loss also decreases the efficiency of treatments, such as chemotherapy in cancer patients. Fighting against muscle loss is thus a major goal for ameliorating patients’ health. Compelling data have demonstrated that increased proteolysis is often the primary factor leading to muscle wasting. However, muscle atrophy is a highly coordinated process that implies the concomitant regulation of anabolic and catabolic pathways, which suggests that studies ought not to be restricted to to proteolysis. Therefore, a potential strategy to improve patients’ condition is to minimize muscle wasting by regulating either proteolysis, protein synthesis or both.

This Special Issue will gather recent insights into the mechanisms driving muscle atrophy, welcoming both original and review articles.

Dr. Daniel Taillandier
Guest Editor

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Keywords

  • muscle atrophy
  • human diseases
  • proteolysis
  • protein synthesis
  • proteolytic systems system
  • therapeutic strategies

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Published Papers (3 papers)

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Research

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21 pages, 5324 KiB  
Article
Triptolide, a Cancer Cell Proliferation Inhibitor, Causes Zebrafish Muscle Defects by Regulating Notch and STAT3 Signaling Pathways
by Byongsun Lee, Yongjin Park, Younggwang Lee, Seyoung Kwon and Jaekyung Shim
Int. J. Mol. Sci. 2024, 25(9), 4675; https://doi.org/10.3390/ijms25094675 - 25 Apr 2024
Viewed by 1113
Abstract
Triptolide is a natural compound in herbal remedies with anti-inflammatory and anti-proliferative properties. We studied its effects on critical signaling processes within the cell, including Notch1 and STAT3 signaling. Our research showed that triptolide reduces cancer cell proliferation by decreasing the expression of [...] Read more.
Triptolide is a natural compound in herbal remedies with anti-inflammatory and anti-proliferative properties. We studied its effects on critical signaling processes within the cell, including Notch1 and STAT3 signaling. Our research showed that triptolide reduces cancer cell proliferation by decreasing the expression of downstream targets of these signals. The levels of each signal-related protein and mRNA were analyzed using Western blot and qPCR methods. Interestingly, inhibiting one signal with a single inhibitor alone did not significantly reduce cancer cell proliferation. Instead, MTT assays showed that the simultaneous inhibition of Notch1 and STAT3 signaling reduced cell proliferation. The effect of triptolide was similar to a combination treatment with inhibitors for both signals. When we conducted a study on the impact of triptolide on zebrafish larvae, we found that it inhibited muscle development and interfered with muscle cell proliferation, as evidenced by differences in the staining of myosin heavy chain and F-actin proteins in confocal fluorescence microscopy. Additionally, we noticed that inhibiting a single type of signaling did not lead to any significant muscle defects. This implies that triptolide obstructs multiple signals simultaneously, including Notch1 and STAT3, during muscle development. Chemotherapy is commonly used to treat cancer, but it may cause muscle loss due to drug-related adverse reactions or other complex mechanisms. Our study suggests that anticancer agents like triptolide, inhibiting essential signaling pathways including Notch1 and STAT3 signaling, may cause muscle atrophy through anti-proliferative activity. Full article
(This article belongs to the Special Issue Muscle Atrophy: From Bench to Bedside 2.0)
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15 pages, 2728 KiB  
Article
Targeting Molecular Mechanisms of Obesity- and Type 2 Diabetes Mellitus-Induced Skeletal Muscle Atrophy with Nerve Growth Factor
by Lauren Jun, Xiao-Wen Ding, Megan Robinson, Hassan Jafari, Emily Knight, Thangiah Geetha, Michael W. Greene and Jeganathan Ramesh Babu
Int. J. Mol. Sci. 2024, 25(8), 4307; https://doi.org/10.3390/ijms25084307 - 13 Apr 2024
Cited by 1 | Viewed by 1305
Abstract
Skeletal muscle plays a critical role in metabolic diseases, such as obesity and type 2 diabetes mellitus (T2DM). Muscle atrophy, characterized by a decrease in muscle mass and function, occurs due to an imbalance between the rates of muscle protein synthesis and degradation. [...] Read more.
Skeletal muscle plays a critical role in metabolic diseases, such as obesity and type 2 diabetes mellitus (T2DM). Muscle atrophy, characterized by a decrease in muscle mass and function, occurs due to an imbalance between the rates of muscle protein synthesis and degradation. This study aimed to investigate the molecular mechanisms that lead to muscle atrophy in obese and T2DM mouse models. Additionally, the effect of nerve growth factor (NGF) on the protein synthesis and degradation pathways was examined. Male mice were divided into three groups: a control group that was fed a standard chow diet, and two experimental groups that were fed a Western diet. After 8 weeks, the diabetic group was injected with streptozotocin to induce T2DM. Each group was then further divided into NGF-treated or non-treated control group. In the gastrocnemius muscles of the Western diet group, increased expressions of myostatin, autophagy markers, and ubiquitin ligases were observed. Skeletal muscle tissue morphology indicated signs of muscle atrophy in both obese and diabetic mice. The NGF-treated group showed a prominent decrease in the protein levels of myostatin and autophagy markers. Furthermore, the NGF-treated group showed an increased Cyclin D1 level. Western diet-induced obesity and T2DM may be linked to muscle atrophy through upregulation of myostatin and subsequent increase in the ubiquitin and autophagy systems. Moreover, NGF treatment may improve muscle protein synthesis and cell cycling. Full article
(This article belongs to the Special Issue Muscle Atrophy: From Bench to Bedside 2.0)
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Review

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16 pages, 1360 KiB  
Review
Aging Skeletal Muscles: What Are the Mechanisms of Age-Related Loss of Strength and Muscle Mass, and Can We Impede Its Development and Progression?
by Thomas Gustafsson and Brun Ulfhake
Int. J. Mol. Sci. 2024, 25(20), 10932; https://doi.org/10.3390/ijms252010932 - 11 Oct 2024
Viewed by 1774
Abstract
As we age, we lose muscle strength and power, a condition commonly referred to as sarcopenia (ICD-10-CM code (M62.84)). The prevalence of sarcopenia is about 5–10% of the elderly population, resulting in varying degrees of disability. In this review we emphasise that sarcopenia [...] Read more.
As we age, we lose muscle strength and power, a condition commonly referred to as sarcopenia (ICD-10-CM code (M62.84)). The prevalence of sarcopenia is about 5–10% of the elderly population, resulting in varying degrees of disability. In this review we emphasise that sarcopenia does not occur suddenly. It is an aging-induced deterioration that occurs over time and is only recognised as a disease when it manifests clinically in the 6th–7th decade of life. Evidence from animal studies, elite athletes and longitudinal population studies all confirms that the underlying process has been ongoing for decades once sarcopenia has manifested. We present hypotheses about the mechanism(s) underlying this process and their supporting evidence. We briefly review various proposals to impede sarcopenia, including cell therapy, reducing senescent cells and their secretome, utilising targets revealed by the skeletal muscle secretome, and muscle innervation. We conclude that although there are potential candidates and ongoing preclinical and clinical trials with drug treatments, the only evidence-based intervention today for humans is exercise. We present different exercise programmes and discuss to what extent the interindividual susceptibility to developing sarcopenia is due to our genetic predisposition or lifestyle factors. Full article
(This article belongs to the Special Issue Muscle Atrophy: From Bench to Bedside 2.0)
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