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活性氧物种与年龄相关基因 p66shc、Sirtuin、FOXO03 和 Klotho 在衰老中的作用。

Reactive oxygen species and age-related genes p66shc, Sirtuin, FOX03 and Klotho in senescence.

机构信息

Vitamin Research Institute; Moscow, Russia.

出版信息

Oxid Med Cell Longev. 2010 Mar-Apr;3(2):77-85. doi: 10.4161/oxim.3.2.11050.

DOI:10.4161/oxim.3.2.11050
PMID:20716932
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2952092/
Abstract

Reactive oxygen species (ROS) superoxide and hydrogen peroxide perform important signaling functions in many physiological and pathophysiological processes. Cell senescence and organismal age are not exemptions.Aging-regulating genes p66shc, Sirtuin, FOXO3a and Klotho are new important factors which are stimulated by ROS signaling. It has been shown that ROS participate in initiation and prolongation of gene-dependent aging development.ROS also participate in the activation of protein kinases Akt/PKB and extracellular signal-regulated kinase ERK, which by themselves or through gene activation stimulates or retards cell senescence.Different retarding/stimulating effects of ROS might depend on the nature of signaling species-superoxide or hydrogen peroxide. Importance of radical anion superoxide as a signaling molecule with"super-nucleophilic" properties points to the possibility of the use of superoxide scavengers (SOD mimetics, ubiquinones and flavonoids) for retarding the development of aging.

摘要

活性氧(ROS)超氧自由基和过氧化氢在许多生理和病理生理过程中发挥着重要的信号功能。细胞衰老和机体衰老也不例外。ROS 信号调节的衰老调节基因 p66shc、Sirtuin、FOXO3a 和 Klotho 是新的重要因素。已经表明,ROS 参与了基因依赖性衰老发展的启动和延长。ROS 还参与蛋白激酶 Akt/PKB 和细胞外信号调节激酶 ERK 的激活,这些激酶本身或通过基因激活刺激或延缓细胞衰老。ROS 的不同延缓/刺激作用可能取决于信号物质超氧自由基或过氧化氢的性质。作为具有“超亲核”特性的信号分子的自由基阴离子超氧自由基的重要性表明,使用超氧阴离子清除剂(SOD 模拟物、泛醌和类黄酮)来延缓衰老发展是可能的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/06d01bf45177/oxim0302_0077_fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/11e9012874c4/oxim0302_0077_fig001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/d9ccc41176b5/oxim0302_0077_fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/7c0253abd026/oxim0302_0077_fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/7e516db3f74d/oxim0302_0077_fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/06d01bf45177/oxim0302_0077_fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/11e9012874c4/oxim0302_0077_fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/3bc794dc8362/oxim0302_0077_fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/9571c223fae6/oxim0302_0077_fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/71d4ca66d56f/oxim0302_0077_fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/d9ccc41176b5/oxim0302_0077_fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/7c0253abd026/oxim0302_0077_fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/7e516db3f74d/oxim0302_0077_fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1dae/2952092/06d01bf45177/oxim0302_0077_fig008.jpg

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