근감소증의 in vitro/in vivo 모델

초록

The etiologies of sarcopenia are not fully understood because the molecular mechanisms of these phenomena are complex and interrelated. Multiple factors of sarcopenia have been identified, including cellular senescence, oxidative stress, mitochondrial dysfunction, fat accumulation, low-grade inflammation, inadequate nutrition, hormonal changes as well as a reduction in the number and regenerating capacity of satellite cells. As there is no single key and inherent cause of sarcopenia, understanding the mechanisms of skeletal muscle aging might be essential for sarcopenia prevention and defining the therapeutic strategies of new drug discovery. Herein, we discuss the fundamental aging mechanisms leading to sarcopenia, summarize the in vitro and in vivo experimental models used to define the molecular and cellular changes in skeletal muscle aging, and provide potential strategies for prevention and treatment of sarcopenia as well as approaches for further development of anti-sarcopenia therapeutics. Fundamental aging mechanisms that contribute to sarcopenia include, but not limited to cellular senescence, inflammation, satellite cell dysfunction, oxidative stress and mitochondrial dysfunction, and dysregulation of protein synthesis and degradation. To represent the mechanisms of sarcopenia, various in vitro models were introduced, including use of reactive oxygen species (e.g., H2O2), ceramide or palmitate, inflammatory cytokines, and glucocorticoid. As in vivo models, use of natural aged animals might be the best model of aging-induced sarcopenia, however animal models with natural aging are time-consuming and not highly cost-effective. Therefore, animal strains with accelerated aging such as senescence-accelerated mice can be used. To elucidate a specific pathogenic mechanism, genetic engineered mice can be used, although the model often show appearance features not seen under normal aging. Based on the molecular mechanisms of sarcopenia, several in vitro models