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Accelerated sarcopenia in Cu/Zn superoxide dismutase knockout mice.
Neuron-specific deletion of CuZnSOD leads to an advanced sarcopenic phenotype in older mice.
Cancer cachexia in a mouse model of oxidative stress.
The in vivo gene expression signature of oxidative stress.
The Geropathology Grading Platform demonstrates that mice null for Cu/Zn-superoxide dismutase show accelerated biological aging.
Oxidative stress-induced dysregulation of excitation-contraction coupling contributes to muscle weakness.
Neuron specific reduction in CuZnSOD is not sufficient to initiate a full sarcopenia phenotype.
A new mouse model of frailty: the Cu/Zn superoxide dismutase knockout mouse.
Does overexpressing Cu/Zn superoxide dismutase retard aging in rodents
Scavenging mitochondrial hydrogen peroxide by peroxiredoxin 3 overexpression attenuates contractile dysfunction and muscle atrophy in a murine model of accelerated sarcopenia.
Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma.
Superoxide Dismutase 1