CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice
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Mitochondrial oxidative stress in aging and healthspanSkeletal Muscle Satellite Cells, Mitochondria, and MicroRNAs: Their Involvement in the Pathogenesis of ALSElevated hydrogen peroxide and decreased catalase and glutathione peroxidase protection are associated with aging sarcopeniaThe lack of CuZnSOD leads to impaired neurotransmitter release, neuromuscular junction destabilization and reduced muscle strength in mice.Superoxide dismutase 1 loss disturbs intracellular redox signaling, resulting in global age-related pathological changes.Muscle-derived extracellular signal-regulated kinases 1 and 2 are required for the maintenance of adult myofibers and their neuromuscular junctions.Can endurance exercise preconditioning prevention disuse muscle atrophy?Redox regulation of muscle adaptations to contractile activity and aging.Sod1 gene ablation in adult mice leads to physiological changes at the neuromuscular junction similar to changes that occur in old wild-type mice.Liver specific expression of Cu/ZnSOD extends the lifespan of Sod1 null mice.Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype.Mitochondrial ROS regulate oxidative damage and mitophagy but not age-related muscle fiber atrophyLong-term administration of the mitochondria-targeted antioxidant mitoquinone mesylate fails to attenuate age-related oxidative damage or rescue the loss of muscle mass and function associated with aging of skeletal muscle.Neuron-specific expression of CuZnSOD prevents the loss of muscle mass and function that occurs in homozygous CuZnSOD-knockout miceRevisiting an age-old question regarding oxidative stress.Redox homeostasis and age-related deficits in neuromuscular integrity and function.Role of reactive oxygen species in age-related neuromuscular deficits.Role of nerve-muscle interactions and reactive oxygen species in regulation of muscle proteostasis with ageing.Denervated muscle fibers induce mitochondrial peroxide generation in neighboring innervated fibers: Role in muscle aging.Comparison of Whole Body SOD1 Knockout with Muscle-Specific SOD1 Knockout Mice Reveals a Role for Nerve Redox Signaling in Regulation of Degenerative Pathways in Skeletal Muscle.Protein S-glutathionylation lowers superoxide/hydrogen peroxide release from skeletal muscle mitochondria through modification of complex I and inhibition of pyruvate uptake.Smoke-induced neuromuscular junction degeneration precedes the fibre type shift and atrophy in COPD.A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse.
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CuZnSOD gene deletion targeted to skeletal muscle leads to loss of contractile force but does not cause muscle atrophy in adult mice
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article científic
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artigo científico
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bilimsel makale
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scientific article published on 31 May 2013
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CuZnSOD gene deletion targeted ...... e muscle atrophy in adult mice
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CuZnSOD gene deletion targeted ...... muscle atrophy in adult mice.
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CuZnSOD gene deletion targeted ...... e muscle atrophy in adult mice
@en
CuZnSOD gene deletion targeted ...... muscle atrophy in adult mice.
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CuZnSOD gene deletion targeted ...... e muscle atrophy in adult mice
@en
CuZnSOD gene deletion targeted ...... muscle atrophy in adult mice.
@nl
P2093
P2860
P356
P1433
P1476
CuZnSOD gene deletion targeted ...... e muscle atrophy in adult mice
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P2093
Anna C Kayani
Anne McArdle
Arlan Richardson
Arunabh Bhattacharya
Carol Davis
Daniel Pulliam
George K Sakellariou
Susan V Brooks
Yiqiang Zhang
P2860
P304
P356
10.1096/FJ.13-228130
P407
P577
2013-05-31T00:00:00Z