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Metabolic regulation of lifespan from a C. elegans perspective.
Genes and Nutrition ( IF 3.5 ) Pub Date : 2019-08-15 , DOI: 10.1186/s12263-019-0650-x
Kathrine B Dall 1 , Nils J Færgeman 1
Affiliation  

Decline of cellular functions especially cognitive is a major deficit that arises with age in humans. Harnessing the strengths of small and genetic tractable model systems has revealed key conserved regulatory biochemical and signaling pathways that control aging. Here, we review some of the key signaling and biochemical pathways that coordinate aging processes with special emphasis on Caenorhabditis elegans as a model system and discuss how nutrients and metabolites can regulate lifespan by coordinating signaling and epigenetic programs. We focus on central nutrient-sensing pathways such as mTOR and insulin/insulin-like growth factor signaling and key transcription factors including the conserved basic helix-loop-helix transcription factor HLH-30/TFEB.

中文翻译:

从秀丽隐杆线虫的角度来看寿命的代谢调节。

细胞功能尤其是认知能力的下降是人类随着年龄增长而出现的主要缺陷。利用小型和遗传易处理模型系统的优势,揭示了控制衰老的关键保守的调节生化和信号通路。在这里,我们回顾了一些协调衰老过程的关键信号传导和生化途径,特别强调秀丽隐杆线虫作为模型系统,并讨论营养物质和代谢物如何通过协调信号传导和表观遗传程序来调节寿命。我们专注于中央营养感应通路,例如 mTOR 和胰岛素/胰岛素样生长因子信号传导以及关键转录因子,包括保守的碱性螺旋-环-螺旋转录因子 HLH-30/TFEB。
更新日期:2020-04-22
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