运动诱导细胞自噬在老年肌少症康复中的研究进展

Regulatory Role of Exercise-induced Autophagy in Rehabilitation of Sarcopenia(review)

老年肌少症是一种与衰老相关的疾病,由于蛋白质合成和降解两者之间的不平衡,导致骨骼肌肉的质量和强度的降低。细胞自噬作为调节体内蛋白质代谢平衡的保守机制,能够被运动诱导的腺苷酸活化蛋白激酶(AMPK)、胰岛素样生长因子(IGF)/蛋白激酶B (Akt)/哺乳动物雷帕霉素靶蛋白(mTOR)及磷脂酰肌醇3激酶(PI3K)/Akt/mTOR等多条信号通路途径调节。而运动激活的细胞自噬调控不同生理病理条件下骨骼肌重塑与内环境稳态的稳定,是骨骼肌健康维持的关键。本文总结不同运动诱导的细胞自噬在老年肌少症的预防、治疗和康复中的作用与潜在的分子机制。

Sarcopenia is an aging-related disease with a significant reduction in mass and strength of skeletal muscle due to the imbalance between protein synthesis and degradation. Autophagy acts as a conserved mechanism regulating the balance of protein metabolism in body and can be regulated by multiple signaling pathways such as AMP-activated protein kinase (AMPK), insulin like growth factor (IGF)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) and phos-phatidylinositol 3 kinase (PI3K)/Akt/mTOR induced by exercise. Exercise-activated autophagy regulates skeletal muscle remodeling and homeostasis under different physiological and pathological conditions, which is the key to skeletal muscle health maintenance. This article reviewed the regulator roles and potential molecular mechanisms of varying exercise-induced autophagy in the prevention, treatment and rehabilitation of sarcopenia.