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首页> 外文期刊>Aging cell. >Longevity and skeletal muscle mass: the role of IGF signalling, the sirtuins, dietary restriction and protein intake
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Longevity and skeletal muscle mass: the role of IGF signalling, the sirtuins, dietary restriction and protein intake

机译：长寿和骨骼肌质量：IGF信号传导，sirtuins，饮食限制和蛋白质摄入的作用

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Advancing age is associated with a progressive loss of skeletal muscle (SkM) mass and function. Given the worldwide aging demographics, this is a major contributor to morbidity, escalating socio-economic costs and ultimately mortality. Previously, it has been established that a decrease in regenerative capacity in addition to SkM loss with age coincides with suppression of insulin/insulin-like growth factor signalling pathways. However, genetic or pharmacological modulations of these highly conserved pathways have been observed to significantly enhance life and healthspan in various species, including mammals. This therefore provides a controversial paradigm in which reduced regenerative capacity of skeletal muscle tissue with age potentially promotes longevity of the organism. This paradox will be assessed and considered in the light of the following: (i) the genetic knockout, overexpression and pharmacological models that induce lifespan extension (e.g. IRS-1/s6K KO, mTOR inhibition) versus the important role of these signalling pathways in SkM growth and adaptation; (ii) the role of the sirtuins (SIRTs) in longevity versus their emerging role in SkM regeneration and survival under catabolic stress; (iii) the role of dietary restriction and its impact on longevity versus skeletal muscle mass regulation; (iv) the crosstalk between cellular energy metabolism (AMPK/TSC2/SIRT1) and survival (FOXO) versus growth and repair of SkM (e.g. AMPK vs. mTOR); and (v) the impact of protein feeding in combination with dietary restriction will be discussed as a potential intervention to maintain SkM mass while increasing longevity and enabling healthy aging.
机译：年龄的增长与骨骼肌（SkM）质量和功能的逐步丧失有关。鉴于全球人口老龄化，这是发病率，社会经济成本不断上升甚至最终导致死亡率的主要因素。以前，已经确定，随着年龄的增长，除SkM丢失外，再生能力的下降与胰岛素/胰岛素样生长因子信号通路的抑制相吻合。然而，已经观察到这些高度保守的途径的遗传或药理学调节显着提高了包括哺乳动物在内的各种物种的生命和健康。因此，这提供了一个有争议的范例，其中随着年龄增长骨骼肌组织的再生能力降低，可能会促进生物体的寿命。将根据以下方面评估和考虑这一悖论：（i）诱导寿命延长的基因敲除，过表达和药理模型（例如IRS-1 / s6K KO，mTOR抑制）与这些信号通路在体内的重要作用SkM的生长和适应; （ii）sirtuins（SIRTs）在长寿中的作用与其在分解代谢应激下在SkM再生和存活中的新兴作用; （iii）饮食限制的作用及其对长寿与骨骼肌质量调节的影响; （iv）细胞能量代谢（AMPK / TSC2 / SIRT1）与生存（FOXO）与SkM的生长和修复（例如AMPK与mTOR）之间的串扰; （v）将讨论蛋白质喂养与饮食限制相结合的影响，作为维持SkM量，增加寿命和促进健康衰老的潜在干预措施。

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