Inducible and reversible SOD2 knockdown in mouse skeletal muscle drives impaired pyruvate oxidation and reduced metabolic flexibility.
Abstract
Skeletal muscle mitochondrial dysfunction is a key characteristic of aging muscle and contributes to age related diseases such as sarcopenia, frailty, and type 2 diabetes. Mitochondrial oxidative stress has been implicated as a driving factor in these age-related diseases, however whether it is a cause, or a consequence of mitochondrial dysfunction remains to be determined. The development of flexible genetic models is an important tool to test the mechanistic role of mitochondrial oxidative stress on skeletal muscle metabolic dysfunction. We characterize a new model of inducible and reversible mitochondrial redox stress using a tetracycline controlled skeletal muscle specific short hairpin RNA targeted to superoxide dismutase 2 (iSOD2).
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Research summary
The paper addresses mitochondrial dysfunction in skeletal muscle, which is a significant factor in aging and age-related diseases. By developing a model to study the role of oxidative stress in metabolic dysfunction, it contributes to understanding the mechanisms underlying aging. However, while the research is solid, it does not present groundbreaking findings that would significantly advance the field, thus the impact score is limited.
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