sirt1介导的能量剥夺(热量限制和运动)对抗肌肉减少症的机制

Wang Jinyue
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摘要

背景:肌肉减少症是肌肉老化的一种症状,其特征是质量损失和力量损失。这种疾病是导致老年人丧失行为能力/死亡的主要原因,也是健康老龄化的大敌。能量剥夺(热量限制和运动)是对抗衰老最有效的手段,而SIRT1是一个关键的中介分子。目的:综述并分析sirt1介导的能量剥夺对抗骨骼肌减少症/骨骼肌衰老的机制。方法:文献复习。结论:运动和热量限制分别导致肌肉的间歇性和持续性能量剥夺,其作用和机制可能存在一定差异。SIRT1可能集中存在于能量剥夺对抗肌肉减少症。AMPK/NAD+是能量剥夺和SIRT1激活之间的桥梁。SIRT1下游主要通过FOXO1/自噬、PGC-1α/线粒体生成、P53/凋亡和DNA修复、NF-κB/炎症4条通路拮抗肌肉老化/肌少症。未来需要关注的方向有:(1)运动和热量限制应激下SIRT1表达机制的差异。(2) SIRT1的非转录因子靶点如eNOS、LKB1等的作用3)同时参与多个细胞事件分子的精确分工,如FOXO1、NF-κB、P53等。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanism of SIRT1-mediated Energy Deprivation (Calorie Restriction and Exercise) Against Sarcopenia
BACKGROUND: Sarcopenia is a symptom of muscle aging characterized by mass loss and strength loss. The disorder is the leading cause of fall incapacity/death in the elderly and the great enemy of healthy aging. Energy deprivation (calorie restriction and exercise) is the most effective means against aging and SIRT1 is a key mediator molecule. OBJECTIVE: The article summarizes and analyzes the mechanisms of SIRT1-mediated energy deprivation against sarcopenia/skeletal muscle aging. METHODS: Literature review. CONCLUSIONS: Exercise and Calorie restriction lead to intermittent and continuous energy deprivation in muscle, respectively, which may contribute to some differences in their effects and mechanisms. SIRT1 may reside centrally in energy deprivation against sarcopenia. AMPK/NAD+ is the bridge between energy deprivation and SIRT1 activation. SIRT1 downstream is mainly through four pathways (FOXO1/autophagy, PGC-1α/mitochondrial generation, P53/apoptosis and DNA repair, and NF-κB/inflammation) to antagonize muscle aging/sarcopenia. Future directions to focus on: (1) Difference between the mechanisms of SIRT1 under stresses of exercise and calorie restriction. (2) The role of non-transcription factor targets of SIRT1 such as eNOS, LKB1, etc. 3) Exact division of labor involved in several cellular event molecules simultaneously, such as FOXO1, NF-κB and P53.
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