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Contribution of energy dysfunction to impaired protein translation in neurodegenerative diseases
Frontiers in Cellular Neuroscience ( IF 4.2 ) Pub Date : 2021-07-09 , DOI: 10.3389/fncel.2021.668500
Yu-Ju Liu , Yijuang Chern

Impaired energy homeostasis and aberrant translational control have independently been implicated in the pathogenesis of neurodegenerative diseases. AMP kinase (AMPK), regulated by the ratio of cellular AMP and ATP, is a major gatekeeper for cellular energy homeostasis. Abnormal regulation of AMPK has been reported in several neurodegenerative diseases, including Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). Most importantly, AMPK activation is known to suppress the translational machinery by inhibiting the mechanistic target of rapamycin complex 1 (mTORC1), activating translational regulators, and phosphorylating nuclear transporter factors. In this review, we describe recent findings on the emerging role of protein translation impairment caused by energy dysregulation in neurodegenerative diseases.

中文翻译:

能量功能障碍对神经退行性疾病中蛋白质翻译受损的贡献

受损的能量稳态和异常的翻译控制已独立地与神经退行性疾病的发病机制有关。AMP 激酶 (AMPK) 受细胞 AMP 和 ATP 的比例调节,是细胞能量稳态的主要看门人。AMPK 的异常调节已在多种神经退行性疾病中报道,包括阿尔茨海默病 (AD) 和肌萎缩侧索硬化症 (ALS)。最重要的是,已知 AMPK 激活通过抑制雷帕霉素复合物 1 (mTORC1) 的机制靶点、激活翻译调节因子和磷酸化核转运因子来抑制翻译机制。在这篇综述中,我们描述了最近关于由能量失调引起的蛋白质翻译障碍在神经退行性疾病中的新作用的发现。
更新日期:2021-07-09
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