AGING CELL:如何缓解年龄相关的肌纤维损伤和损失?

2019-04-03 海北 MedSci原创

衰老导致骨骼肌萎缩(即肌肉减少症),肌纤维损失是该过程的关键组成部分。然而,至今为止,这些与年龄相关的变化背后的机制仍不清楚。

衰老导致骨骼肌萎缩(即肌肉减少症),肌纤维损失是该过程的关键组成部分。然而,至今为止,这些与年龄相关的变化背后的机制仍不清楚。

最近,研究人员发现,mTORC1信号在老化小鼠和人类的骨骼肌纤维子集中被激活,与纤维损伤共定位。在TSC1敲除的小鼠肌肉纤维中,mTORC1的激活增加了形态异常线粒体的含量,并且在衰老期间引起进行性氧化应激,纤维损伤和纤维损失。

转录组分析显示,mTORC1的激活增加了生长分化因子(GDF3,5和15)以及参与线粒体氧化应激和分解代谢的基因的表达。研究人员表示,增加的GDF15足以诱导氧化应激和分解代谢变化,并且mTORC1通过STAT3的磷酸化增加GDF15的表达。

老年小鼠中mTORC1的抑制降低了GDFs的表达,以及STAT3在骨骼肌中的磷酸化,减少了氧化应激和肌纤维损伤或损失。

因此,长期增加的mTORC1活性有助于与年龄相关的肌肉萎缩,并且GDF信号传导是该实验提出的机制。


原始出处:

Huibin Tang et al. mTORC1 underlies age‐related muscle fiber damage and loss by inducing oxidative stress and catabolism. AGING CELL, 2019; doi: https://doi.org/10.1111/acel.12943


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    2020-01-09 维他命
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    2019-11-27 okhuali
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    2019-04-03 蝴蝶A

    学习了,涨知识了

    0

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