scholarly journals Molecular Mechanisms Controlling Skeletal Muscle Mass

10.5772/60876 ◽  
2015 ◽  
Author(s):  
Kunihiro Sakuma ◽  
Akihiko Yamaguchi
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms

scholarly journals Molecular Mechanisms Regulating Skeletal Muscle Mass

2019 ◽  
Vol 54 (2) ◽  
pp. 133-142
Author(s):  
Senay Akin ◽  
◽  
Berkay Ozerklig ◽  
Ibrahim Turkel ◽  
Haydar A. Demirel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms

scholarly journals p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Barbé ◽  
Audrey Loumaye ◽  
Pascale Lause ◽  
Olli Ritvos ◽  
Jean-Paul Thissen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Molecular Mechanisms ◽  
Muscle Development ◽  
The Body ◽  
Negative Regulator ◽  
Skeletal Muscle Hypertrophy ◽  
Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

scholarly journals Skeletal Muscle Recovery from Disuse Atrophy: Protein Turnover Signaling and Strategies for Accelerating Muscle Regrowth

2020 ◽  
Vol 21 (21) ◽  
pp. 7940
Author(s):  
Timur M. Mirzoev
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Mechanical Loading ◽  
Protein Turnover ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Muscle Recovery ◽  
Mechanical Unloading

Skeletal muscle fibers have a unique capacity to adjust their metabolism and phenotype in response to alternations in mechanical loading. Indeed, chronic mechanical loading leads to an increase in skeletal muscle mass, while prolonged mechanical unloading results in a significant decrease in muscle mass (muscle atrophy). The maintenance of skeletal muscle mass is dependent on the balance between rates of muscle protein synthesis and breakdown. While molecular mechanisms regulating protein synthesis during mechanical unloading have been relatively well studied, signaling events implicated in protein turnover during skeletal muscle recovery from unloading are poorly defined. A better understanding of the molecular events that underpin muscle mass recovery following disuse-induced atrophy is of significant importance for both clinical and space medicine. This review focuses on the molecular mechanisms that may be involved in the activation of protein synthesis and subsequent restoration of muscle mass after a period of mechanical unloading. In addition, the efficiency of strategies proposed to improve muscle protein gain during recovery is also discussed.

Downregulation of Akt/mammalian target of rapamycin pathway in skeletal muscle is associated with increased REDD1 expression in response to chronic hypoxia

2010 ◽  
Vol 298 (6) ◽  
pp. R1659-R1666 ◽  
Author(s):  
François B. Favier ◽  
Frédéric Costes ◽  
Aurélia Defour ◽  
Régis Bonnefoy ◽  
Etienne Lefai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms ◽  
Chronic Hypoxia ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Pathway ◽  
Target Of Rapamycin ◽  
Strong Increase ◽  
Copd Patients

Although it is well established that chronic hypoxia leads to an inexorable loss of skeletal muscle mass in healthy subjects, the underlying molecular mechanisms involved in this process are currently unknown. Skeletal muscle atrophy is also an important systemic consequence of chronic obstructive pulmonary disease (COPD), but the role of hypoxemia in this regulation is still debated. Our general aim was to determine the molecular mechanisms involved in the regulation of skeletal muscle mass after exposure to chronic hypoxia and to test the biological relevance of our findings into the clinical context of COPD. Expression of positive and negative regulators of skeletal muscle mass were explored 1) in the soleus muscle of rats exposed to severe hypoxia (6,300 m) for 3 wk and 2) in vastus lateralis muscle of nonhypoxemic and hypoxemic COPD patients. In rodents, we observed a marked inhibition of the mammalian target of rapamycin (mTOR) pathway together with a strong increase in regulated in development and DNA damage response 1 (REDD1) expression and in its association with 14-3-3, a mechanism known to downregulate the mTOR pathway. Importantly, REDD1 overexpression in vivo was sufficient to cause skeletal muscle fiber atrophy in normoxia. Finally, the comparative analysis of skeletal muscle in hypoxemic vs. nonhypoxemic COPD patients confirms that hypoxia causes an inhibition of the mTOR signaling pathway. We thus identify REDD1 as a negative regulator of skeletal muscle mass during chronic hypoxia. Translation of this fundamental knowledge into the clinical investigation of COPD shows the interest to develop therapeutic strategies aimed at inhibiting REDD1.

scholarly journals Recent progress toward understanding the molecular mechanisms that regulate skeletal muscle mass

2011 ◽  
Vol 23 (12) ◽  
pp. 1896-1906 ◽  
Author(s):  
Craig A. Goodman ◽  
David L. Mayhew ◽  
Troy A. Hornberger
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Recent Progress ◽  
Molecular Mechanisms

Translational Control of Protein Synthesis: Implications for Understanding Changes in Skeletal Muscle Mass

2001 ◽  
Vol 11 (s1) ◽  
pp. S143-S149 ◽  
Author(s):  
Leonard S. Jefferson ◽  
Scot R. Kimball
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Translation Initiation ◽  
Translational Control ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Protein ◽  
Ribosomal Subunit ◽  
Mrna Binding

Gain or loss of skeletal muscle mass is due largely to the establishment of an imbalance between rates of protein synthesis and degradation. A key determinant of the rate of protein synthesis is translation initiation, a process regulated in part through binding of initiator methionyl-tRNA (met-tRNAi) and messenger RNA (mRNA) to a 40S ribosomal subunit. Either the met-tRNAi or mRNA binding step can become limiting for protein synthesis. Furthermore, the mRNA binding step can modulate translation of specific mRNAs with or without changes in the overall rate of protein synthesis. This report highlights molecular mechanisms involved in mediating control of the mRNA binding step in translation initiation. Particular attention is given to the effect of exercise on this step and to how the branched-chain amino acid leucine stimulates muscle protein synthesis after exercise. Potential mechanisms for exercise induced increase in muscle mass are discussed.

scholarly journals Molecular Regulation of Skeletal Muscle Growth and Organelle Biosynthesis: Practical Recommendations for Exercise Training

2021 ◽  
Vol 22 (5) ◽  
pp. 2741
Author(s):  
Robert Solsona ◽  
Laura Pavlin ◽  
Henri Bernardi ◽  
Anthony MJ Sanchez
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Mass ◽  
Ribosome Biogenesis ◽  
Skeletal Muscle Mass ◽  
Molecular Mechanisms ◽  
Muscle Growth ◽  
Mtorc1 Pathway ◽  
Practical Recommendations

The regulation of skeletal muscle mass and organelle homeostasis is dependent on the capacity of cells to produce proteins and to recycle cytosolic portions. In this investigation, the mechanisms involved in skeletal muscle mass regulation—especially those associated with proteosynthesis and with the production of new organelles—are presented. Thus, the critical roles of mammalian/mechanistic target of rapamycin complex 1 (mTORC1) pathway and its regulators are reviewed. In addition, the importance of ribosome biogenesis, satellite cells involvement, myonuclear accretion, and some major epigenetic modifications related to protein synthesis are discussed. Furthermore, several studies conducted on the topic of exercise training have recognized the central role of both endurance and resistance exercise to reorganize sarcomeric proteins and to improve the capacity of cells to build efficient organelles. The molecular mechanisms underlying these adaptations to exercise training are presented throughout this review and practical recommendations for exercise prescription are provided. A better understanding of the aforementioned cellular pathways is essential for both healthy and sick people to avoid inefficient prescriptions and to improve muscle function with emergent strategies (e.g., hypoxic training). Finally, current limitations in the literature and further perspectives, notably on epigenetic mechanisms, are provided to encourage additional investigations on this topic.

Androgenic and estrogenic regulation of skeletal muscle mass and atrophy signaling in male mice

2013 ◽  
Author(s):  
Naeyer Helene De ◽  
Inge Everaert ◽  
Spaey Annelies De ◽  
Jean-Marc Kaufman ◽  
Youri Taes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Male Mice ◽  
Estrogenic Regulation

The BMI and skeletal muscle mass as a risk factor of carotid atherosclerosis in patients with type 2 diabetes

2018 ◽  
Author(s):  
Se-Hwa Kim ◽  
Soo-Kyung Kim ◽  
Young-Ju Choi ◽  
Seok-Won Park ◽  
Eun-Jig Lee ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Risk Factor ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Carotid Atherosclerosis

771-P: Protein Intake at Breakfast Contributes to Maintenance of Skeletal Muscle Mass in Japanese Elderly Patients with Type 2 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 771-P
Author(s):  
SODAI KUBOTA ◽  
HITOSHI KUWATA ◽  
SAKI OKAMOTO ◽  
DAISUKE YABE ◽  
KENTA MUROTANI ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Elderly Patients ◽  
Muscle Mass ◽  
Protein Intake ◽  
Skeletal Muscle Mass ◽  
P Protein ◽  
Japanese Elderly
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