Disuse-induced muscle wasting.
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TLDR
The current understanding of the molecular and cellular mechanisms regulating muscle loss under disuse conditions are examined, discussing the similarities and areas of dispute between the animal and human literature.About:
This article is published in The International Journal of Biochemistry & Cell Biology.The article was published on 2013-10-01 and is currently open access. It has received 270 citations till now. The article focuses on the topics: Muscle atrophy & Atrophy.read more
Citations
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Skeletal muscle atrophy during short-term disuse: Implications for age-related sarcopenia
TL;DR: Research is warranted to elucidate the physiological and molecular basis for rapid muscle loss during short periods of disuse, which will allow the characterization of nutritional, exercise and/or pharmacological interventions to prevent or attenuate Muscle loss during periods ofdisuse and therefore aid in the treatment of age-related sarcopenia.
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An Antibody Blocking Activin Type II Receptors Induces Strong Skeletal Muscle Hypertrophy and Protects from Atrophy
Estelle Lach-Trifilieff,Giulia Minetti,Kelly-Ann Sheppard,Chikwendu Ibebunjo,Jerome N. Feige,Steffen Hartmann,Sophie Brachat,Helene Rivet,Claudia Koelbing,Frederic Morvan,Shinji Hatakeyama,David J. Glass +11 more
TL;DR: A novel, human anti-ActRII antibody is developed to prevent binding of ligands to the receptors and thus inhibit downstream signaling in the myostatin/activin type II receptor pathway, highlighting the compelling therapeutic potential of BYM338 for the treatment of skeletal muscle atrophy and weakness in multiple settings.
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MicroRNAs in metabolism
TL;DR: This review emphasizes current ideas and controversies within miRNA research in metabolism, and emphasizes their importance as both endocrine signalling molecules and potentially disease markers.
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Hindlimb unloading: rodent analog for microgravity.
TL;DR: Key HU results for various organ systems including those related to stress; the immune, cardiovascular, and nervous systems; vision changes; and wound healing are examined.
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Muscle Atrophy Induced by Mechanical Unloading: Mechanisms and Potential Countermeasures
TL;DR: Current and potential therapeutic countermeasures that have shown promising results in preventing and restoring disuse-induced muscle loss are elaborated and what are the key challenges in this field as well as some future prospectives are identified.
References
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Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
Anne Brunet,Azad Bonni,Michael J. Zigmond,Michael Z. Lin,Peter Juo,Linda Hu,Michael J. Anderson,Karen C. Arden,John Blenis,Michael E. Greenberg +9 more
TL;DR: It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
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The Ubiquitin-Proteasome Proteolytic Pathway: Destruction for the Sake of Construction
TL;DR: It is clear now that degradation of cellular proteins is a highly complex, temporally controlled, and tightly regulated process that plays major roles in a variety of basic pathways during cell life and death as well as in health and disease.
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Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy
Sue C. Bodine,Esther Latres,Susanne Baumhueter,Venus Lai,Lorna Nunez,Brian A. Clarke,William Poueymirou,Frank J. Panaro,Erqian Na,Kumar Dharmarajan,Zhen-Qiang Pan,David M. Valenzuela,Thomas M. DeChiara,Trevor Stitt,George D. Yancopoulos,David J. Glass +15 more
TL;DR: Two genes encode ubiquitin ligases that are potential drug targets for the treatment of muscle atrophy, and mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy.
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Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy
Marco Sandri,Claudia Sandri,Alexander Gilbert,Carsten Skurk,Elisa Calabria,Anne Picard,Kenneth Walsh,Stefano Schiaffino,Stewart H. Lecker,Alfred L. Goldberg +9 more
TL;DR: It is shown that in cultured myotubes undergoing atrophy, the activity of the PI3K/AKT pathway decreases, leading to activation of Foxo transcription factors and atrogin-1 induction.
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Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.
Sue C. Bodine,Trevor Stitt,Michael Gonzalez,William O. Kline,Gretchen L. Stover,Roy Bauerlein,Elizabeth Zlotchenko,Angus Scrimgeour,John C. Lawrence,David J. Glass,George D. Yancopoulos +10 more
TL;DR: It is concluded that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of this pathway can oppose muscle atrophy induced by disuse.