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자료유형
학술저널
저자정보
서대윤 (인제대학교) 배준현 (서울대학교) 방현석 (동명대학교) 곽이섭 (동의대학교)
저널정보
한국운동생리학회 운동과학 운동과학 제29권 제3호
발행연도
2020.1
수록면
202 - 207 (6page)

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PURPOSE: Skeletal muscle atrophy induces overall health problems and many related diseases in older adults. In particular, sarcopeniais related to lowered quality of life, decreased physical activity, high levels of morbidity and mortality owing to chronic diseases, andeven falling. Despite the many clinical studies on skeletal muscle atrophy, a little study had been about the exact mechanism of skeletalmuscle atrophy at the molecular level. In 2017, A disease code (ICD-10-CM) for skeletal muscle atrophy related to sarcopenia wasannounced to attempt a clinical approach in the United States. According to these approaches, non-invasive clinical treatment is themost effective method for treating skeletal muscle atrophy. The purpose of this study was to analyze the molecular mechanisms of muscularexercise and related skeletal muscle atrophy factors. METHODS: This systemic review focused on skeletal muscle atrophy and muscular exercise. The keywords were used on “MeSH: muscleatrophy OR skeletal muscle atrophy OR muscle OR atrophy AND physical exercise OR exercise OR exercise training” for Englishand Korean. This paper searched PubMED, OVIDMEDLINE, and EMBASE for literature consideration. RESULTS: Skeletal muscle atrophy was related to a complex molecular network, and exercise affects IGF-1/Akt/mTOR signaling. Therelated skeletal muscle atrophy factors were evaluated as MurF1, MAFbx, IGF-1, and NFkB. We proposed new related factors such asATF 4, Gadd45a, and p21; however, the results related to exercise were not shown in recent studies. CONLCUSIONS: In conclusion, we identified skeletal muscle atrophy factors at the molecular level of muscle physiology, and thesenew factors may become an interesting field of study in clinical human trial and animal studies.

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