Role of skeletal muscle homeostasis of functional food material

2020 ◽  
Vol 155 (4) ◽  
pp. 236-240
Author(s):  
Toshiko Yamazawa ◽  
Shizuo Yamada
Keyword(s):  
Skeletal Muscle ◽  
Functional Food ◽  
Food Material ◽  
Muscle Homeostasis

scholarly journals The Role of Eif6 in Skeletal Muscle Homeostasis Revealed by Endurance Training Co-expression Networks

Cell Reports ◽  
2017 ◽  
Vol 21 (6) ◽  
pp. 1507-1520 ◽  
Author(s):  
Kim Clarke ◽  
Sara Ricciardi ◽  
Tim Pearson ◽  
Izwan Bharudin ◽  
Peter K. Davidsen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Muscle Homeostasis

The role of AMP-activated protein kinase in the coordination of skeletal muscle turnover and energy homeostasis

2012 ◽  
Vol 303 (5) ◽  
pp. C475-C485 ◽  
Author(s):  
Anthony M. J. Sanchez ◽  
Robin B. Candau ◽  
Alfredo Csibi ◽  
Allan F. Pagano ◽  
Audrey Raibon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Energy Homeostasis ◽  
Therapeutic Potential ◽  
Energy Status ◽  
Muscle Plasticity ◽  
Glucose And Lipid Metabolism ◽  
Muscle Homeostasis ◽  
Amp Activated Protein Kinase

The AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase that acts as a sensor of cellular energy status switch regulating several systems including glucose and lipid metabolism. Recently, AMPK has been implicated in the control of skeletal muscle mass by decreasing mTORC1 activity and increasing protein degradation through regulation of ubiquitin-proteasome and autophagy pathways. In this review, we give an overview of the central role of AMPK in the control of skeletal muscle plasticity. We detail particularly its implication in the control of the hypertrophic and atrophic signaling pathways. In the light of these cumulative and attractive results, AMPK appears as a key player in regulating muscle homeostasis and the modulation of its activity may constitute a therapeutic potential in treating muscle wasting syndromes in humans.

Role of Mitochondrial Calcium in the Maintenance of Skeletal Muscle Homeostasis

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Anna Raffaello ◽  
Simona Feno ◽  
Denis Vecellio Reane ◽  
Fabio Munari ◽  
Francesca Vallese ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Calcium ◽  
Muscle Homeostasis

scholarly journals mTORC2 affects the maintenance of the muscle stem cell pool

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nathalie Rion ◽  
Perrine Castets ◽  
Shuo Lin ◽  
Leonie Enderle ◽  
Judith R. Reinhard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mammalian Target Of Rapamycin ◽  
Adult Skeletal Muscle ◽  
Muscle Stem Cells ◽  
And Function ◽  
Muscle Homeostasis ◽  
Biological Methods

Abstract Background The mammalian target of rapamycin complex 2 (mTORC2), containing the essential protein rictor, regulates cellular metabolism and cytoskeletal organization by phosphorylating protein kinases, such as PKB/Akt, PKC, and SGK. Inactivation of mTORC2 signaling in adult skeletal muscle affects its metabolism, but not muscle morphology and function. However, the role of mTORC2 in adult muscle stem cells (MuSCs) has not been investigated. Method Using histological, biochemical, and molecular biological methods, we characterized the muscle phenotype of mice depleted for rictor in the Myf5-lineage (RImyfKO) and of mice depleted for rictor in skeletal muscle fibers (RImKO). The proliferative and myogenic potential of MuSCs was analyzed upon cardiotoxin-induced injury in vivo and in isolated myofibers in vitro. Results Skeletal muscle of young and 14-month-old RImyfKO mice appeared normal in composition and function. MuSCs from young RImyfKO mice exhibited a similar capacity to proliferate, differentiate, and fuse as controls. In contrast, the number of MuSCs was lower in young RImyfKO mice than in controls after two consecutive rounds of cardiotoxin-induced muscle regeneration. Similarly, the number of MuSCs in RImyfKO mice decreased with age, which correlated with a decline in the regenerative capacity of mutant muscle. Interestingly, reduction in the number of MuSCs was also observed in 14-month-old RImKO muscle. Conclusions Our study shows that mTORC2 signaling is dispensable for myofiber formation, but contributes to the homeostasis of MuSCs. Loss of mTORC2 does not affect their myogenic function, but impairs the replenishment of MuSCs after repeated injuries and their maintenance during aging. These results point to an important role of mTORC2 signaling in MuSC for muscle homeostasis.

scholarly journals The ubiquitin–proteasome system in regulation of the skeletal muscle homeostasis and atrophy: from basic science to disorders

2020 ◽  
Vol 70 (1) ◽  
Author(s):  
Yasuo Kitajima ◽  
Kiyoshi Yoshioka ◽  
Naoki Suzuki
Keyword(s):  
Skeletal Muscle ◽  
Protein Degradation ◽  
Ubiquitin Proteasome System ◽  
Intracellular Protein ◽  
Muscle Stem Cells ◽  
Muscle Diseases ◽  
Intracellular Protein Degradation ◽  
Ubiquitin Proteasome ◽  
Muscle Homeostasis

Abstract Skeletal muscle is one of the most abundant and highly plastic tissues. The ubiquitin–proteasome system (UPS) is recognised as a major intracellular protein degradation system, and its function is important for muscle homeostasis and health. Although UPS plays an essential role in protein degradation during muscle atrophy, leading to the loss of muscle mass and strength, its deficit negatively impacts muscle homeostasis and leads to the occurrence of several pathological phenotypes. A growing number of studies have linked UPS impairment not only to matured muscle fibre degeneration and weakness, but also to muscle stem cells and deficiency in regeneration. Emerging evidence suggests possible links between abnormal UPS regulation and several types of muscle diseases. Therefore, understanding of the role of UPS in skeletal muscle may provide novel therapeutic insights to counteract muscle wasting, and various muscle diseases. In this review, we focussed on the role of proteasomes in skeletal muscle and its regeneration, including a brief explanation of the structure of proteasomes. In addition, we summarised the recent findings on several diseases and elaborated on how the UPS is related to their pathological states.

scholarly journals Role of Mitochondrial Calcium in the Maintenance of Skeletal Muscle Homeostasis

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Anna Raffaello ◽  
Denis Vecellio Reane ◽  
Carlo Reggiani
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Calcium ◽  
Muscle Homeostasis

scholarly journals Role of Inflammation in Muscle Homeostasis and Myogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Domiziana Costamagna ◽  
Paola Costelli ◽  
Maurilio Sampaolesi ◽  
Fabio Penna
Keyword(s):  
Skeletal Muscle ◽  
Muscle Wasting ◽  
Regulatory Pathways ◽  
Effective Strategies ◽  
Rapid Changes ◽  
Intracellular Pathways ◽  
Definition Of ◽  
Muscle Homeostasis ◽  
Myogenic Program

Skeletal muscle mass is subject to rapid changes according to growth stimuli inducing both hypertrophy, through increased protein synthesis, and hyperplasia, activating the myogenic program. Muscle wasting, characteristic of several pathological states associated with local or systemic inflammation, has been for long considered to rely on the alteration of myofiber intracellular pathways regulated by both hormones and cytokines, eventually leading to impaired anabolism and increased protein breakdown. However, there are increasing evidences that even alterations of the myogenic/regenerative program play a role in the onset of muscle wasting, even though the precise mechanisms involved are far from being fully elucidated. The comprehension of the links potentially occurring between impaired myogenesis and increased catabolism would allow the definition of effective strategies aimed at counteracting muscle wasting. The first part of this review gives an overview of skeletal muscle intracellular pathways determining fiber size, while the second part considers the cells and the regulatory pathways involved in the myogenic program. In both parts are discussed the evidences supporting the role of inflammation in impairing muscle homeostasis and myogenesis, potentially determining muscle atrophy.

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