A cytoprotective perspective on longevity regulation.

A cytoprotective perspective on longevity regulation.
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DOI:
10.1016/j.tcb.2013.04.007
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发表时间:
2013-09
影响因子:
19
通讯作者:
Ruvkun, Gary
Ruvkun, Gary
中科院分区:
生物学1区
文献类型:
--
作者:
Shore, David E.;Ruvkun, Gary

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延长寿命的机制有很多,包括胰岛素/IGF-1信号、代谢、翻译或摄食的破坏。尽管这些途径的功能不同,但抑制每一种途径都会引起缓冲压力和损伤的反应。在这里,我们强调秀丽隐杆线虫的遗传分析数据,我们探索了作为长寿计划主要元素激活的许多细胞保护机制的效应物和上游调控成分,包括解毒、先天免疫、蛋白质平衡和氧化应激反应。我们表明,它们的诱导支持了跨功能不同触发因素和跨物种的寿命延长。细胞保护途径与长寿的进化交织在一起,与核心细胞成分的监测相结合,在对药物、化学物质和病原体的正常和异常反应中具有重要意义。
There are many mechanisms of lifespan extension, including the disruption of insulin/IGF-1 signaling, metabolism, translation, or feeding. Despite the disparate functions of these pathways, inhibition of each induces responses that buffer stress and damage. Here, emphasizing data from genetic analyses in C. elegans, we explore the effectors and upstream regulatory components of numerous cytoprotective mechanisms activated as major elements of longevity programs, including detoxification, innate immunity, proteostasis, and oxidative stress response. We show that their induction underpins longevity extension across functionally diverse triggers and across species. Intertwined with the evolution of longevity, cytoprotective pathways are coupled to the surveillance of core cellular components, with important implications in normal and aberrant responses to drugs, chemicals, and pathogens.
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