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Open AccessJournal ArticleDOI

Protein breakdown in muscle wasting: role of autophagy-lysosome and ubiquitin-proteasome.

Marco Sandri
- 01 Oct 2013 - 
- Vol. 45, Iss: 10, pp 2121-2129
TLDR
This review will focus on the last progress in ubiquitin-proteasome and autophagy-lysosome systems and their involvement in muscle atrophy.
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 514 citations till now. The article focuses on the topics: Muscle atrophy & Skeletal muscle.

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Cancer-associated cachexia

TL;DR: Cachexia is a disorder characterized by loss of body weight with specific losses of skeletal muscle and adipose tissue as mentioned in this paper, which is associated with cancers of the pancreas, oesophagus, stomach, lung, liver and bowel.
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ROS and Autophagy: Interactions and Molecular Regulatory Mechanisms

TL;DR: The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation, which includes various molecular signal pathways such as ROS–FOXO3–LC3/BNIP3–autophagy, ROS–NRF2–P62–autPhagy, Ros–HIF1–BNIP1/NIX–aut Phagy, and ROS–TIGAR–autphagy.
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Signaling pathways controlling skeletal muscle mass.

TL;DR: The relevant recent literature demonstrating these previously undiscovered mediators governing anabolism and catabolism of skeletal muscle, as well as the signaling events that induce differentiation and post-injury regeneration, are summarized and discussed.
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Mechanisms of muscle wasting in chronic kidney disease

TL;DR: Myostatin inhibition could yield new therapeutic directions for blocking muscle protein wasting in CKD or disorders associated with its complications, suggesting that therapeutic strategies will be developed to suppress or block protein loss.
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Mitochondrial dysfunction and sarcopenia of aging: From signaling pathways to clinical trials

TL;DR: This review summarizes prominent findings and controversial issues on the contribution of specific mitochondrial processes - including oxidative stress, quality control mechanisms and apoptotic signaling - on the development of sarcopenia and presents methodological and safety considerations for the design of clinical trials targeting mitochondrial dysfunction to treat sarc Openia.
References
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Autophagy: Renovation of Cells and Tissues

TL;DR: It is explored how recent mouse models in combination with advances in human genetics are providing key insights into how the impairment or activation of autophagy contributes to pathogenesis of diverse diseases, from neurodegenerative diseases such as Parkinson disease to inflammatory disorders such as Crohn disease.
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Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1

TL;DR: PGC-1, a cold-inducible coactivator of nuclear receptors, stimulates mitochondrial biogenesis and respiration in muscle cells through an induction of uncoupling protein 2 (UCP-2) and through regulation of the nuclear respiratory factors (NRFs).
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p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy

TL;DR: It is demonstrated that the previously reported aggresome-like induced structures containing ubiquitinated proteins in cytosolic bodies are dependent on p62 for their formation and p62 is required both for the formation and the degradation of polyubiquitin-containing bodies by autophagy.
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Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy

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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