Search results for "MUSCLE ATROPHY"

showing 10 items of 47 documents

Abnormalities of mitochondrial functioning can partly explain the metabolic disorders encountered in sarcopenic gastrocnemius.

2007

International audience; Aging triggers several abnormalities in muscle glycolytic fibers including increased proteolysis, reactive oxygen species (ROS) production and apoptosis. Since the mitochondria are the main site of substrate oxidation, ROS production and programmed cell death, we tried to know whether the cellular disorders encountered in sarcopenia are due to abnormal mitochondrial functioning. Gastrocnemius mitochondria were extracted from adult (6 months) and aged (21 months) male Wistar rats. Respiration parameters, opening of the permeability transition pore and ROS production, with either glutamate (amino acid metabolism) or pyruvate (glucose metabolism) as a respiration substr…

Malemuscle atrophyMESH : Cell Aging[SDV]Life Sciences [q-bio]MESH : Reactive Oxygen SpeciesMitochondrion0302 clinical medicineGlycolysisMESH: AnimalsMESH : Muscle SkeletalMESH : Fatty AcidsCellular SenescencePhospholipidsMESH: Superoxide Dismutasereactive oxygen speciesMESH : Free Radicals0303 health sciencesMESH: Muscle SkeletalMESH : RatsFatty Acidsfatty acid profile of mitochondrial lipidsMESH: Reactive Oxygen SpeciesPyruvate dehydrogenase complexMESH: Fatty Acidsmitochondria[SDV] Life Sciences [q-bio]BiochemistryMESH: Cell AgingMESH: CalciumMESH : MitochondriaCell agingPyruvate decarboxylationmedicine.medical_specialtyFree RadicalsMESH: RatsCellular respirationMESH: MitochondriaMESH : MaleCell Respirationchemistry.chemical_elementOxidative phosphorylationBiologyCalciumMESH : Rats WistarMESH : Phospholipids03 medical and health sciencesMESH: Free RadicalsInternal medicinemedicineAnimalsMESH : Superoxide DismutaseRats WistarMuscle SkeletalMESH : Calcium030304 developmental biologyMESH: Phospholipidscalciumpermeability transition poreSuperoxide Dismutaseagingaging;calcium;fatty acid profile of mitochondrial lipids;mitochondria;muscle atrophy;permeability transition pore;reactive oxygen species;Animals;Calcium;Cell Aging;Cell Respiration;Fatty Acids;Free Radicals;Male;Mitochondria;Muscle;Skeletal;Phospholipids;Rats;Wistar;Reactive Oxygen Species;Superoxide DismutaseCell BiologyMESH: Rats WistarMESH: MaleRatsEndocrinologychemistryMESH : Cell RespirationMESH : AnimalsMESH: Cell Respiration030217 neurology & neurosurgery
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Whey proteins are more efficient than casein in the recovery of muscle functional properties following a casting induced muscle atrophy.

2013

International audience; The purpose of this study was to investigate the effect of whey supplementation, as compared to the standard casein diet, on the recovery of muscle functional properties after a casting-induced immobilization period. After an initial (I0) evaluation of the contractile properties of the plantarflexors (isometric torque-frequency relationship, concentric power-velocity relationship and a fatigability test), the ankle of 20 male adult rats was immobilized by casting for 8 days. During this period, rats were fed a standard diet with 13% of casein (CAS). After cast removal, rats received either the same diet or a diet with 13% of whey proteins (WHEY). A control group (n =…

Malemuscle atrophyimmobilization periodlcsh:MedicineIsometric exerciseConcentric0302 clinical medicinecasein dietFracture FixationCaseinlcsh:Science0303 health sciencesMultidisciplinaryCaseinsOrgan SizeMilk ProteinsMuscle atrophyatrophie musculairerégime alimentaireMuscular AtrophyimmobilisationBiochemistryHomogeneousAlimentation et NutritionMuscle Fatiguemedicine.symptomMuscle ContractionResearch ArticleMuscle contractionBiology03 medical and health sciencesAnimal scienceIsometric Contractionmedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]Food and NutritionAnimalsPower outputMuscle Skeletal030304 developmental biologycaséineMuscle fatigueBody Weightlcsh:Rcasein diet;whey proteins;muscle atrophy;immobilization periodDietRatswhey proteinsDietary Supplementsprotéine du petit laitlcsh:Q[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryPLoS ONE
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Differentiation of Murine C2C12 Myoblasts Strongly Reduces the Effects of Myostatin on Intracellular Signaling

2020

Alongside in vivo models, a simpler and more mechanistic approach is required to study the effects of myostatin on skeletal muscle because myostatin is an important negative regulator of muscle size. In this study, myostatin was administered to murine (C2C12) and human (CHQ) myoblasts and myotubes. Canonical and noncanonical signaling downstream to myostatin, related ligands, and their receptor were analyzed. The effects of tumorkines were analyzed after coculture of C2C12 and colon cancer-C26 cells. The effects of myostatin on canonical and noncanonical signaling were strongly reduced in C2C12 cells after differentiation. This may be explained by increased follistatin, an endogenous blocke…

Muscle Fibers Skeletallcsh:QR1-502lihaksetlcsh:MicrobiologyArticleTGF-BETA SUPERFAMILYCell LineMyoblastsMicetumorkineCell Line TumorfollistatinAnimalsHumansCANCER CACHEXIAskeletal muscleMUSCLE ATROPHYlihassolutSmadsoluviestintäRECEPTORCell DifferentiationIN-VITROMyostatinmusculoskeletal systemMAPKActivinsLEUKEMIA INHIBITORY FACTORACTIVIN-AinflammationCulture Media ConditionedCELLSPROTEIN-SYNTHESISmyotubeGROWTH1182 Biochemistry cell and molecular biologyproteiinit3111 BiomedicinecocultureSignal Transduction
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Inactivity-induced oxidative stress: A central role in age-related sarcopenia?

2012

Ageing causes a progressive decline in skeletal muscle mass that may lead to decreased strength and functionality. The term sarcopenia is especially used to characterise this geriatric syndrome. Numerous conditions and behaviours are considered to accelerate the progression of sarcopenia such as chronic diseases, malnutrition and physical inactivity. As people in modern countries are more and more sedentary, the impact of physical inactivity on the prevalence of sarcopenia might be more and more important in the future. In this review, we discuss how reactive oxygen species (ROS) could mediate the effects of lifelong inactivity in the onset and progression of age-related sarcopenia. Althoug…

Sarcopeniamedicine.medical_specialty[SDV]Life Sciences [q-bio]Physical Therapy Sports Therapy and RehabilitationMotor ActivityBiologymedicine.disease_causeInternal medicinemedicineHumansOrthopedics and Sports MedicineAge-related sarcopeniaComputingMilieux_MISCELLANEOUSAgedAged 80 and over2. Zero hungerchemistry.chemical_classificationReactive oxygen speciesSkeletal muscleGeneral Medicinemedicine.diseaseMuscle atrophy3. Good healthMuscular AtrophyOxidative StressMalnutritionmedicine.anatomical_structureEndocrinologychemistryAgeingSarcopeniamedicine.symptomOxidative stressSignal TransductionEuropean Journal of Sport Science
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Decreased motor unit firing rate and force control in older men

2006

Introduction Ageing is related to muscle atrophy that leads to decreases in muscle force. The largest changes are found in fast muscle fibres and fast force production, reducing the capability to recover from sudden balance disturbances. Also ageing-related decrease in force control has been found, as indicated by an increase in force fluctuations and motor unit (MU) firing variability (Galganski et al. 1993). Possibly due to differences in measurement protocols and muscles, the results concerning the effects of ageing on motor unit firing rate are, however, somewhat contradictory (for review, see Roos et al. 1997). The purpose of the present study was to investigate the age-related changes…

Soleus musclemedicine.medical_specialtyChemistryPhysical Therapy Sports Therapy and RehabilitationMuscle atrophyMotor unitPhysical medicine and rehabilitationMotor unit firing rateAgeingmedicinePhysical therapyOrthopedics and Sports Medicinemedicine.symptomBalance impairmentBalance (ability)Muscle forceJapanese Journal of Physical Fitness and Sports Medicine
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Redox regulation of E3 ubiquitin ligases and their role in skeletal muscle atrophy

2015

Muscle atrophy is linked to reactive oxygen species (ROS) production during hindlimb-unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of our study was to determine the mechanism by which ROS cause muscle atrophy and its possible prevention by allopurinol, a well-known inhibitor of XO widely used in clinical practice, and indomethacin, a nonsteroidal anti-inflammatory drug. We studied the activation of p38 MAP Kinase and NF-?B pathways, and the expression of two E3 ubiquitin ligases involved in proteolysis, the Muscle atrophy F-Box (MAFb) and Muscle RING Finger-1 (MuRF-1). Male Wistar rats (3 mold) conditioned by 14 days of hindlimb unloading (n=18),…

Soleus musclemedicine.medical_specialtySkeletal muscleAllopurinolHindlimbBiologymedicine.disease_causemedicine.diseaseBiochemistryMuscle atrophychemistry.chemical_compoundmedicine.anatomical_structureEndocrinologyAtrophychemistryBiochemistryPhysiology (medical)Internal medicinemedicinemedicine.symptomXanthine oxidaseOxidative stressmedicine.drugFree Radical Biology and Medicine
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Dexamethasone Inhibits the Pro-Angiogenic Potential of Primary Human Myoblasts

2021

Tissue regeneration depends on the complex processes of angiogenesis, inflammation and wound healing. Regarding muscle tissue, glucocorticoids (GCs) inhibit pro-inflammatory signalling and angiogenesis and lead to muscle atrophy. Our hypothesis is that the synthetic GC dexamethasone (dex) impairs angiogenesis leading to muscle atrophy or inhibited muscle regeneration. Therefore, this study aims to elucidate the effect of dexamethasone on HUVECs under different conditions in mono- and co-culture with myoblasts to evaluate growth behavior and dex impact with regard to muscle atrophy and muscle regeneration. Viability assays, qPCR, immunofluorescence as well as ELISAs were performed on HUVECs,…

Vascular Endothelial Growth Factor A0301 basic medicineMuscle tissueCD31endocrine systemQH301-705.5AngiogenesisMyoblasts SkeletalNeovascularization PhysiologicInflammationdexamethasonehuman primary myoblastsArticleCatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicineHuman Umbilical Vein Endothelial Cellsmedicinepolycyclic compoundsHumansMyocyteBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyHUVECsTube formationChemistryOrganic ChemistryGeneral Medicineco-cultureVEGFCoculture TechniquesMuscle atrophyComputer Science ApplicationsCell biologyChemistry030104 developmental biologymedicine.anatomical_structureGene Expression RegulationCD31medicine.symptomWound healing030217 neurology & neurosurgeryhormones hormone substitutes and hormone antagonistsInternational Journal of Molecular Sciences
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Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy through miR-7 biogenesis repression

2021

Skeletal muscle symptoms strongly contribute to mortality of myotonic dystrophy type 1 (DM1) patients. DM1 is a neuromuscular genetic disease caused by CTG repeat expansions that, upon transcription, sequester the Muscleblind-like family of proteins and dysregulate alternative splicing of hundreds of genes. However, mis-splicing does not satisfactorily explain muscle atrophy and wasting, and several other contributing factors have been suggested, including hyperactivated autophagy leading to excessive catabolism. MicroRNA ( miR ) -7 has been demonstrated to be necessary and sufficient to repress the autophagy pathway in cell models of the disease, but the origin of its low levels in DM1 was…

autophagyMSI2 antisense oligonucleotides autophagy miR-7 muscle atrophy muscle dysfunction myotonic dystrophy myotubesRM1-950BiologyMyotonic dystrophyMSI2chemistry.chemical_compoundDrug DiscoverymedicineMyocyteGene silencingMBNL1muscle dysfunctionmyotonic dystrophyMyogenesisAutophagymiR-7Skeletal musclemedicine.diseaseMuscle atrophyCell biologymedicine.anatomical_structurechemistryMolecular MedicineTherapeutics. Pharmacologyantisense oligonucleotidesmedicine.symptomMolecular Therapy - Nucleic Acids
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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OGT and OGA expression in postmenopausal skeletal muscle associates with hormone replacement therapy and muscle cross-sectional area

2013

Protein glycosylation via O-linked N-acetylglucosaminylation (O-GlcNAcylation) is an important post-translational regulatory mechanism mediated by O-GlcNAc transferase (OGT) and responsive to nutrients and stress. OGT attaches an O-GlcNAc moiety to proteins, while O-GlcNAcase (OGA) catalyzes O-GlcNAc removal. In skeletal muscle of experimental animals, prolonged increase in O-GlcNAcylation associates with age and muscle atrophy. Here we examined the effects of hormone replacement therapy (HRT) and power training (PT) on muscle OGT and OGA gene expression in postmenopausal women generally prone to age-related muscle weakness. In addition, the associations of OGT and OGA gene expressions with…

medicine.medical_specialtyAgingGlycosylationTime Factorsmedicine.drug_classPlyometric ExerciseBiologyta3111N-AcetylglucosaminyltransferasesBiochemistryGene Expression Regulation EnzymologicEndocrinologyDownregulation and upregulationInternal medicineGene expressionGeneticsmedicineHumansMuscle StrengthRNA Messengerta315Muscle SkeletalMolecular BiologyFinlandGlyceraldehyde 3-phosphate dehydrogenasePlyometric power trainingEstrogen Replacement Therapyta1182Age FactorsMuscle weaknessSkeletal muscleta3141Cell BiologyMiddle Agedbeta-N-AcetylhexosaminidasesMuscle atrophyPostmenopausePhenotypeTreatment OutcomeEndocrinologymedicine.anatomical_structureEstrogenbiology.proteinFemaleMuscle atrophymedicine.symptomProtein Processing Post-TranslationalMuscle ContractionMuscle contraction
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