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1. Full Text Cellular and molecular mechanisms of muscle atrophy
by Bonaldo, Paolo and Sandri, Marco
DMM Disease Models and Mechanisms, ISSN 1754-8403, 01/2013, Volume 6, Issue 1, pp. 25 - 39
Skeletal muscle is a plastic organ that is maintained by multiple pathways regulating cell and protein turnover. During muscle atrophy, proteolytic systems are... 
MYOBLAST DIFFERENTIATION | GLUCOCORTICOID-RECEPTOR | RETRACTED ARTICLE. SEE | PROTEIN-DEGRADATION | PATHOLOGY | FOXO TRANSCRIPTION FACTORS | RING FINGER 1 | UBIQUITIN LIGASES | ADULT SKELETAL-MUSCLE | GROWTH-FACTOR-I | TRANSGENIC MICE | CELL BIOLOGY | Cytokines - metabolism | Muscular Atrophy - metabolism | Signal Transduction | Humans | Muscular Atrophy - pathology | Ubiquitin - metabolism | Homeostasis | Mice, Transgenic | Muscle, Skeletal - metabolism | Muscular Atrophy - genetics | Autophagy | Mice, Knockout | Animals | Lysosomes - metabolism | Models, Biological | Inflammation Mediators - metabolism | Muscle Proteins - metabolism | Mice | Muscle, Skeletal - pathology | Myostatin - metabolism | Proteasome Endopeptidase Complex - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Muscular Atrophy - etiology | Review
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2. Full Text Mitochondrial signaling contributes to disuse muscle atrophy
by Powers, Scott K and Wiggs, Michael P and Duarte, Jose A and Murat Zergeroglu, A and Demirel, Haydar A
American Journal of Physiology - Endocrinology and Metabolism, ISSN 0193-1849, 07/2012, Volume 303, Issue 1, pp. E31 - E39
Powers SK, Wiggs MP, Duarte JA, Zergeroglu AM, Demirel HA. Mitochondrial signaling contributes to disuse muscle atrophy. Am J Physiol Endocrinol Metab 303:... 
Redox balance | Oxidative stress | Muscle wasting | Cell signaling | ACTIVATION | PHYSIOLOGY | TARGETED ANTIOXIDANTS PROTECT | MECHANICAL VENTILATION | redox balance | DENERVATION | PROTEOLYSIS | muscle wasting | EXERCISE | SKELETAL-MUSCLE | cell signaling | ENDOCRINOLOGY & METABOLISM | INTERMYOFIBRILLAR MITOCHONDRIA | DYSFUNCTION | oxidative stress | Mitochondrial Diseases - pathology | Muscular Disorders, Atrophic - metabolism | Protein Biosynthesis | Muscular Atrophy - metabolism | Oxidative Stress | Signal Transduction | Mitochondria, Muscle - pathology | Humans | Mitochondria, Muscle - metabolism | Muscular Atrophy - pathology | Mitochondrial Diseases - metabolism | Muscle, Skeletal - metabolism | Immobilization - adverse effects | Mitochondrial Diseases - etiology | Animals | Proteolysis | Muscular Disorders, Atrophic - pathology | Muscle, Skeletal - pathology | Muscular Atrophy - etiology | Muscular Disorders, Atrophic - etiology | Disease Models, Animal | Muscles | Physiological aspects | Development and progression | Genetic aspects | Mitochondrial DNA | Health aspects | Atrophy, Muscular | Reviews
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3. Full Text Reversal of Cancer Cachexia and Muscle Wasting by ActRIIB Antagonism Leads to Prolonged Survival
by Zhou, Xiaolan and Wang, Jin Lin and Lu, John and Song, Yanping and Kwak, Keith S and Jiao, Qingsheng and Rosenfeld, Robert and Chen, Qing and Boone, Thomas and Simonet, W. Scott and Lacey, David L and Goldberg, Alfred L and Han, H.Q
Cell, ISSN 0092-8674, 2010, Volume 142, Issue 4, pp. 531 - 543
Muscle wasting and cachexia have long been postulated to be key determinants of cancer-related death, but there has been no direct experimental evidence to... 
CELLBIO | PROTEINS | HUMDISEASE | Proteins | Cellbio | Humdisease | SKELETAL-MUSCLE | ACTIVIN-A | PROTEIN | INHIBIN-DEFICIENT MICE | TUMOR PROGRESSION | ATROPHY | ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | MYOSTATIN | SATELLITE CELL | CELL BIOLOGY | Tumor Necrosis Factor-alpha - metabolism | Neoplasm Transplantation | Cachexia - drug therapy | Humans | Activin Receptors, Type II - antagonists & inhibitors | Activins - metabolism | Male | Transplantation, Heterologous | Neoplasms - complications | Anorexia - drug therapy | Interleukin-1beta - metabolism | Cachexia - etiology | Muscle Proteins - metabolism | Female | Atrophy - drug therapy | Interleukin-6 - metabolism | Muscular Atrophy - etiology | Signal Transduction | Mice, Inbred C57BL | Neoplasms - mortality | Myocardium - pathology | Atrophy - etiology | Muscular Atrophy - drug therapy | Myoblasts - pathology | Mice, Knockout | Animals | Inhibins - metabolism | Activin Receptors, Type II - genetics | Anorexia - etiology | Inhibins - genetics | Mice | Muscle, Skeletal - pathology | Ubiquitin | Prevention | Cell research | Care and treatment | Ligases | Analysis | Stem cells | Cachexia | Cancer
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4. Full Text Rapid Disuse Atrophy of Diaphragm Fibers in Mechanically Ventilated Humans
by Levine, Sanford and Nguyen, Taitan and Taylor, Nyali and Friscia, Michael E and Budak, Murat T and Rothenberg, Pamela and Zhu, Jianliang and Sachdeva, Rajeev and Sonnad, Seema and Kaiser, Larry R and Rubinstein, Neal A and Powers, Scott K and Shrager, Joseph B
The New England Journal of Medicine, ISSN 0028-4793, 03/2008, Volume 358, Issue 13, pp. 1327 - 1335
Weaning patients from mechanical ventilation after modest periods of diaphragmatic inactivity can be difficult. In this study, changes in the cross-sectional... 
SKELETAL-MUSCLE | MEDICINE, GENERAL & INTERNAL | OBSTRUCTIVE PULMONARY-DISEASE | OXIDATIVE STRESS | CYTOKINES | MYOSIN | INJURY | MECHANISMS | EXPRESSION | FAILURE | UBIQUITIN-PROTEASOME PATHWAY | Diaphragm - pathology | SKP Cullin F-Box Protein Ligases - genetics | Humans | Middle Aged | Male | RNA, Messenger - metabolism | Case-Control Studies | Tripartite Motif Proteins | Respiration, Artificial - adverse effects | Muscle Proteins - metabolism | Pectoralis Muscles - anatomy & histology | Adult | Female | Diaphragm - metabolism | Muscular Atrophy - etiology | Brain Death | Gene Expression | Muscular Atrophy - pathology | Ubiquitin-Protein Ligases - metabolism | SKP Cullin F-Box Protein Ligases - metabolism | Diaphragm - anatomy & histology | Muscle Proteins - genetics | Biopsy | Adolescent | Muscle Fibers, Skeletal - pathology | Muscle Fibers, Skeletal - cytology | Aged | Tissue Donors | Ubiquitin-Protein Ligases - genetics | Causes of | Complications and side effects | Atrophy, Muscular | Artificial respiration | Medical research | Ventilation | Methods
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5. Full Text Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy
by Sandri, Marco and Sandri, Claudia and Gilbert, Alex and Skurk, Carsten and Calabria, Elisa and Picard, Anne and Walsh, Kenneth and Schiaffino, Stefano and Lecker, Stewart H and Goldberg, Alfred L
Cell, ISSN 0092-8674, 04/2004, Volume 117, Issue 3, pp. 399 - 412
Skeletal muscle atrophy is a debilitating response to fasting, disuse, cancer, and other systemic diseases. In atrophying muscles, the ubiquitin ligase,... 
HYPERTROPHY | PROTEASOME PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | DAF-16 | GENE-EXPRESSION | DIFFERENTIATION | IDENTIFICATION | NF-KAPPA-B | MAMMALIAN-CELLS | FKHR | CELL BIOLOGY | Ligases - genetics | Protein-Serine-Threonine Kinases | Muscle, Skeletal - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Muscle Cells - enzymology | SKP Cullin F-Box Protein Ligases | Muscle Proteins | RNA Interference | Glucocorticoids - metabolism | Cloning, Molecular | Adenoviridae - genetics | Fasting - metabolism | Muscular Atrophy - etiology | Proto-Oncogene Proteins - metabolism | Promoter Regions, Genetic | Muscular Atrophy - metabolism | Signal Transduction | Cells, Cultured | Gene Expression Regulation | Ubiquitin-Protein Ligases - metabolism | Ligases - metabolism | Muscular Atrophy - genetics | Transcription Factors - genetics | Proto-Oncogene Proteins c-akt | Transcription Factors - metabolism | Animals | Models, Biological | Mice | Muscle, Skeletal - pathology | Genetic Vectors | Insulin-Like Growth Factor I - metabolism | Ligases | Analysis | Genetic transcription
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6. Full Text Sarcopenia: Its assessment, etiology, pathogenesis, consequences and future perspectives
by Rolland, Y and Czerwinski, S and van Kan, G Abellan and Morley, J E and Cesari, M and Onder, G and Woo, J and Baumgartner, R and Pillard, F and Boirie, Y and Chumlea, W M. C and Vellas, B
The Journal of Nutrition Health and Aging, ISSN 1279-7707, 9/2008, Volume 12, Issue 7, pp. 433 - 450
Sarcopenia is a loss of muscle protein mass and loss of muscle function. It occurs with increasing age, being a major component in the development of frailty.... 
Neurosciences | Medicine & Public Health | Nutrition | Geriatrics/Gerontology | Aging | Quality of Life Research | Primary Care Medicine | ACUTE CREATINE SUPPLEMENTATION | NUTRITION & DIETETICS | SKELETAL-MUSCLE MASS | LEAN BODY-MASS | CONVERTING ENZYME-INHIBITION | FAT-FREE MASS | VITAMIN-D-RECEPTOR | LOWER-EXTREMITY PERFORMANCE | RANDOMIZED CONTROLLED-TRIAL | REPORTED FUNCTIONAL LIMITATION | GROWTH-FACTOR-I | GERIATRICS & GERONTOLOGY | Humans | Muscular Atrophy - pathology | Frail Elderly | Muscle, Skeletal - physiology | Aging - physiology | Muscle, Skeletal - physiopathology | Aged, 80 and over | Aged | Exercise - physiology | Muscular Atrophy - prevention & control | Muscular Atrophy - etiology | Muscular Atrophy - epidemiology | Aging - metabolism | Muscle, Skeletal - anatomy & histology
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7. Full Text Oxidative stress and disuse muscle atrophy: cause or consequence?
by Powers, Scott K and Smuder, Ashley J and Judge, Andrew R
Current Opinion in Clinical Nutrition and Metabolic Care, ISSN 1363-1950, 05/2012, Volume 15, Issue 3, pp. 240 - 245
PURPOSE OF REVIEWThis review will discuss the evidence both for and against the concept that reactive oxygen species (ROS) play an important role in the... 
Antioxidants | Oxidants | Calpain | Caspase-3 | Muscle protein synthesis | Proteasome | Reactive oxygen species rebox | muscle protein synthesis | proteasome | ACTIVATION | TARGETED ANTIOXIDANTS PROTECT | antioxidants | SOLEUS MUSCLE | MECHANICAL VENTILATION | HUMANS | KAPPA-B | WEAKNESS | redox | calpain | SKELETAL-MUSCLE | MITOCHONDRIAL ROS | NUTRITION & DIETETICS | reactive oxygen species | ENDOCRINOLOGY & METABOLISM | oxidants | CONTRIBUTES | caspase-3 | Muscular Disorders, Atrophic - metabolism | Muscular Disorders, Atrophic - complications | Reactive Oxygen Species - metabolism | Muscular Atrophy - metabolism | Oxidative Stress | Signal Transduction | Humans | Muscular Atrophy - pathology | Muscle, Skeletal - metabolism | Proteolysis | Muscle Proteins - metabolism | Muscular Disorders, Atrophic - pathology | Muscle, Skeletal - pathology | Muscular Atrophy - etiology
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8. Full Text Rapidly progressive diaphragmatic weakness and injury during mechanical ventilation in humans
by Jaber, Samir and Petrof, Basil J and Jung, Boris and Chanques, Gérald and Berthet, Jean-Philippe and Rabuel, Christophe and Bouyabrine, Hassan and Courouble, Patricia and Koechlin-Ramonatxo, Christelle and Sebbane, Mustapha and Similowski, Thomas and Scheuermann, Valérie and Mebazaa, Alexandre and Capdevila, Xavier and Mornet, Dominique and Mercier, Jacques and Lacampagne, Alain and Philips, Alexandre and Matecki, Stefan
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 02/2011, Volume 183, Issue 3, pp. 364 - 371
Rationale. Diaphragmatic function is a major determinant of the ability to successfully wean patients from mechanical ventilation (MV). Paradoxically, MV... 
Atrophy | Calpain | Diaphragm disuse | Weaning | Ventilator-induced diaphragmatic dysfunction | OXIDATIVE STRESS | ACTIVATION | CALPAIN-3 | CONTRACTILE DYSFUNCTION | MUSCULAR-DYSTROPHY | RAT DIAPHRAGM | diaphragm disuse | weaning | calpain | FIBERS | PIGLET DIAPHRAGM | PATHWAY | RESPIRATORY SYSTEM | atrophy | ventilator-induced diaphragmatic dysfunction | CRITICAL CARE MEDICINE | Muscle Weakness - etiology | Diaphragm - pathology | Diaphragm - chemistry | Humans | Middle Aged | Muscular Atrophy - pathology | Calpain - analysis | Male | Ubiquitinated Proteins - analysis | Diaphragm - injuries | Young Adult | Transcription Factor RelA - analysis | Muscular Atrophy - physiopathology | Respiration, Artificial - adverse effects | Time Factors | Muscle Weakness - pathology | Adult | Female | Muscle Weakness - physiopathology | Muscular Atrophy - etiology | Diaphragm - physiopathology | Life Sciences
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9. Full Text Comparison of multifidus muscle atrophy and trunk extension muscle strength: Percutaneous versus open pedicle screw fixation
by Kim, Dong-Yun and Lee, Sang-Ho and Sang, Ki Chung and Lee, Ho-Yeon
Spine, ISSN 0362-2436, 01/2005, Volume 30, Issue 1, pp. 123 - 129
Study Design. This study was conducted by retrospective case selection and prospective observation of longitudinal changes of the multifidus muscle... 
Pedicle screw | Percutaneous surgery | Multifidus muscle | Lumbar spine | SURGERY | INSTRUMENTATION | LOW-BACK-PAIN | LUMBAR ERECTOR SPINAE | multifidus muscle | STABILIZATION | STABILITY | DISORDERS | CLINICAL NEUROLOGY | pedicle screw | INTERBODY FUSION | percutaneous surgery | SKELETAL FIXATION | lumbar spine | ORTHOPEDICS | PARASPINAL MUSCLES | Spinal Fusion - methods | Postoperative Complications - etiology | Bone Screws | Humans | Middle Aged | Muscular Atrophy - pathology | Male | Treatment Outcome | Muscle, Skeletal - physiology | Spinal Fusion - adverse effects | Spinal Fusion - instrumentation | Spondylolisthesis - surgery | Magnetic Resonance Imaging | Muscle Contraction | Female | Aged | Retrospective Studies | Muscle, Skeletal - pathology | Muscular Atrophy - etiology
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10. Full Text Advanced glycation end‐products induce skeletal muscle atrophy and dysfunction in diabetic mice via a RAGE‐mediated, AMPK‐down‐regulated, Akt pathway
by Chiu, Chen‐Yuan and Yang, Rong‐Sen and Sheu, Meei‐Ling and Chan, Ding‐Cheng and Yang, Ting‐Hua and Tsai, Keh‐Sung and Chiang, Chih‐Kang and Liu, Shing‐Hwa
The Journal of Pathology, ISSN 0022-3417, 02/2016, Volume 238, Issue 3, pp. 470 - 482
Diabetic myopathy, a less studied complication of diabetes, exhibits the clinical observations characterized by a less muscle mass, muscle weakness and a... 
advanced glycation end‐products | alagebrium chloride | diabetic myopathy | advanced glycation end-products | CELLS | REGENERATION | HEART-FAILURE | RATS | PATHOLOGY | NEPHROPATHY | INSULIN | ONCOLOGY | CROSS-LINK BREAKER | FAT DIET | ACCUMULATION | TYPE-1 | AMP-Activated Protein Kinases - metabolism | MAP Kinase Signaling System - physiology | Humans | Atrophy - pathology | Male | Case-Control Studies | Muscular Diseases - etiology | Muscle Proteins - metabolism | Muscle Weakness - pathology | Diabetes Mellitus - etiology | Muscle Fatigue - physiology | Muscle Weakness - etiology | Down-Regulation | Muscular Diseases - pathology | SKP Cullin F-Box Protein Ligases - metabolism | Atrophy - etiology | Muscle, Skeletal - physiology | Regeneration - physiology | Animals | Diabetes Mellitus, Experimental - etiology | Glycation End Products, Advanced - metabolism | Muscle Fibers, Skeletal - pathology | Receptor for Advanced Glycation End Products - physiology | Signal Transduction - physiology | Aged | Mice | Thiazoles - pharmacology | Muscle, Skeletal - pathology | Muscles | Health aspects | Diabetes | Index Medicus
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