Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy

Muller, Florian L.; Song, Wook; Liu, Yuhong; Chaudhuri, Asish; Pieke-Dahl, Sandra; Strong, Randy; Huang, Ting; Epstein, Charles J.; Roberts, L. Jackson; Csete, Marie; Faulkner, John A.; Remmen, Holly Van

doi:10.1016/j.freeradbiomed.2006.01.036

Cited by 388 publications

(472 citation statements)

References 55 publications

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“…The features of the SOD1 −/− mouse model mimic those observed in 30 month old WT mice27, 277 and in older humans 6, 277. In addition, in common with old WT mice, skeletal muscle from SOD1 −/− rodents exhibits increased levels of oxidative damage27, 29, 30, 31, 33, 34, 276, 277 and a constitutive activation of redox‐sensitive transcription factors33; hence, it has been suggested that this knockout murine model represents a useful model for the study of chronic oxidative damage in the context of neuromuscular ageing in an effort to identify potential mechanisms and pathways that underlie sarcopenia in humans. It is noteworthy that hemizygous transgenic mouse models that overexpress CuZnSOD (TgSOD1 +/o ), CAT (TgCAT +/o ) and combined (TgSOD1/CAT +/o ) show no increase in lifespan and fail to rescue age‐related muscle wasting and functional deficits 26…”

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 65%

“…Moreover, although indistinguishable from WT mice at birth, by 5–8 months of age, SOD1 −/− mice show an accelerated neuromuscular ageing phenotype associated with myofibre atrophy (Figure 5), neurological impairments (Figure 6) and functional deficits 275. The features of the SOD1 −/− mouse model mimic those observed in 30 month old WT mice27, 277 and in older humans 6, 277. In addition, in common with old WT mice, skeletal muscle from SOD1 −/− rodents exhibits increased levels of oxidative damage27, 29, 30, 31, 33, 34, 276, 277 and a constitutive activation of redox‐sensitive transcription factors33; hence, it has been suggested that this knockout murine model represents a useful model for the study of chronic oxidative damage in the context of neuromuscular ageing in an effort to identify potential mechanisms and pathways that underlie sarcopenia in humans.…”

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 83%

“…Reduced lifespan observed in SOD1 −/− ,27 PRX1 −/− ,250 PRX2 −/− 251 and TRX2 +/− 252 models is much more prominent in the SOD1 −/− rodent model,281 indicating that specific key RONS regulatory systems and redox signalling pathways are implicated in the processes of ageing. Moreover, although indistinguishable from WT mice at birth, by 5–8 months of age, SOD1 −/− mice show an accelerated neuromuscular ageing phenotype associated with myofibre atrophy (Figure 5), neurological impairments (Figure 6) and functional deficits 275.…”

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 97%

“…SOD1 −/− ,27 PRX1 −/− ,250 PRX2 −/− ,251 TRX2 +/− 252 and MSRA −/− 253 rodent models show a reduction in lifespan; in contrast, more recent studies have reported no effect of MSRA −/− on rodent lifespan 254. GPX1 −/− ,28, 252 SOD2 +/− ,240 extracellular SOD −/− 255, 256 and MSRB −/− 257 knockout murine models show no effect on lifespan.…”

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 99%

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Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 65%

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 83%

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 97%

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 99%

See 2 more Smart Citations

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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“…Oxidative stress has been proposed to play an important role in the initiation and progression of muscle atrophy during aging (Muller et al ., 2006; Jang et al ., 2010). Previous studies have reported elevated antioxidant enzyme activity from treatment with butyrate and HDAC inhibitors (Kang et al ., 2002; Shimazu et al ., 2013).…”

Section: Discussionmentioning

confidence: 99%

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

Walsh¹,

et al. 2015

Self Cite

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SummarySarcopenia, the loss of skeletal muscle mass and function during aging, is a major contributor to disability and frailty in the elderly. Previous studies found a protective effect of reduced histone deacetylase activity in models of neurogenic muscle atrophy. Because loss of muscle mass during aging is associated with loss of motor neuron innervation, we investigated the potential for the histone deacetylase (HDAC) inhibitor butyrate to modulate age‐related muscle loss. Consistent with previous studies, we found significant loss of hindlimb muscle mass in 26‐month‐old C57Bl/6 female mice fed a control diet. Butyrate treatment starting at 16 months of age wholly or partially protected against muscle atrophy in hindlimb muscles. Butyrate increased muscle fiber cross‐sectional area and prevented intramuscular fat accumulation in the old mice. In addition to the protective effect on muscle mass, butyrate reduced fat mass and improved glucose metabolism in 26‐month‐old mice as determined by a glucose tolerance test. Furthermore, butyrate increased markers of mitochondrial biogenesis in skeletal muscle and whole‐body oxygen consumption without affecting activity. The increase in mass in butyrate‐treated mice was not due to reduced ubiquitin‐mediated proteasomal degradation. However, butyrate reduced markers of oxidative stress and apoptosis and altered antioxidant enzyme activity. Our data is the first to show a beneficial effect of butyrate on muscle mass during aging and suggests HDACs contribute to age‐related muscle atrophy and may be effective targets for intervention in sarcopenia and age‐related metabolic disease.

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Development of Animal Models of Drug‐Induced Mitochondrial Toxicity

Boelsterli

Lee

2008

Drug‐Induced Mitochondrial Dysfunction

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Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy

Cited by 388 publications

References 55 publications

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

The histone deacetylase inhibitor butyrate improves metabolism and reduces muscle atrophy during aging

Development of Animal Models of Drug‐Induced Mitochondrial Toxicity

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