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首页> 外文期刊>Cell metabolism >The Unfolded Protein Response Mediates Adaptation to Exercise in Skeletal Muscle through a PGC-1alpha/ATF6alpha Complex.
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The Unfolded Protein Response Mediates Adaptation to Exercise in Skeletal Muscle through a PGC-1alpha/ATF6alpha Complex.

机译：展开的蛋白质反应通过PGC-1alpha / ATF6alpha复合体介导对骨骼肌运动的适应。

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摘要

Exercise has been shown to be effective for treating obesity and type 2 diabetes. However, the molecular mechanisms for adaptation to exercise training are not fully understood. Endoplasmic reticulum (ER) stress has been linked to metabolic dysfunction. Here we show that the unfolded protein response (UPR), an adaptive response pathway that maintains ER homeostasis upon luminal stress, is activated in skeletal muscle during exercise and adapts skeletal muscle to exercise training. The transcriptional coactivator PGC-1alpha, which regulates several exercise-associated aspects of skeletal muscle function, mediates the UPR in myotubes and skeletal muscle through coactivation of ATF6alpha. Efficient recovery from acute exercise is compromised in ATF6alpha(-/-) mice. Blocking ER-stress-related cell death via deletion of CHOP partially rescues the exercise intolerance phenotype in muscle-specific PGC-1alpha KO mice. These findings suggest that modulation of the UPR through PGC1alpha represents an alternative avenue to improve skeletal muscle function and achieve metabolic benefits.
机译：锻炼已被证明可有效治疗肥胖和2型糖尿病。但是，尚未完全了解适应运动训练的分子机制。内质网（ER）应激与代谢功能障碍有关。在这里，我们显示了未折叠的蛋白质反应（UPR），一种适应性反应途径，在腔压力下维持ER稳态，在运动过程中在骨骼肌中被激活，并使骨骼肌适应运动训练。转录共激活因子PGC-1alpha调节骨骼肌功能的几个运动相关方面，通过ATF6alpha的共激活介导肌管和骨骼肌中的UPR。从ATF6alpha（-/-）小鼠急性运动的有效恢复受到损害。通过删除CHOP来阻止内质网应激相关的细胞死亡，部分挽救了肌肉特异性PGC-1alpha KO小鼠的运动耐受性表型。这些发现表明，通过PGC1alpha调节UPR代表了改善骨骼肌功能和获得代谢益处的另一种途径。

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