| Literature DB >> 23851030 |
Aphrodite Vasilaki1, Malcolm J Jackson2.
Abstract
The ability of muscles to regenerate successfully following damage diminishes with age and this appears to be a major contributor to the development of muscle weakness and physical frailty. Successful muscle regeneration is dependent on appropriate reinnervation of regenerating muscle. Age-related changes in the interactions between nerve and muscle are poorly understood but may play a major role in the defective regeneration. During aging there is defective redox homeostasis and an accumulation of oxidative damage in nerve and muscle that may contribute to defective regeneration. The aim of this review is to summarise the evidence that abnormal reactive oxygen species (ROS) generation in nerve and/or muscle may be responsible for the defective regeneration that contributes to the degeneration of skeletal muscle observed during aging. Identifying the importance of ROS generation in skeletal muscle during aging could have fundamental implications for interventions to prevent muscle degeneration and treatments to reverse the age-related decline in muscle mass and function.Entities:
Keywords: AP-1; Aging; CNS; CuZnSOD; GPx1; GSH; HSPs; Innervation; MnSOD; NAD(P)H; NFκB; NMJs; NO; Neuromuscular junction; ROS; Reactive oxygen species; Regeneration; SOD; SOD1; Skeletal muscle; WT; XO; activator protein-1; central nervous system; copper, zinc superoxide dismutase; glutathione peroxidase 1; heat shock proteins; manganese superoxide dismutase; mpcs; myogenic precursor cells; nNOS; neuromuscular junctions; neuronal nitric oxide synthase; nitric oxide; nuclear transcription factor κappa B; reactive oxygen species; reduced glutathione; reduced nicotine adenine dinucleotide phosphate; superoxide dismutase; wild type; xanthine oxidase
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Year: 2013 PMID： 23851030 PMCID： PMC3859734 DOI： 10.1016/j.freeradbiomed.2013.07.008
Source DB: PubMed Journal: Free Radic Biol Med ISSN： 0891-5849 Impact factor: 7.376