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衰老:线粒体的“M”键(此处可意译为“线粒体与衰老的关键联系”之类表述,仅为便于理解,按要求可不添加,直接为)衰老:线粒体相关

Aging: Dial M for Mitochondria.

作者信息

Hur Jae H, Cho Jaehyoung, Walker David W

机构信息

Department of Physiological Science, University of California, Los Angeles, Los Angeles, CA 90095, USA.

出版信息

Aging (Albany NY). 2010 Jan 26;2(1):69-73. doi: 10.18632/aging.100118.

DOI:10.18632/aging.100118
PMID:20228940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2837206/
Abstract

A major goal of aging research is to identify interventions that prolong lifespan in distantly related organisms. In recent years, genetic studies in both nematodes and rodents have reported that moderate inactivation of genes important for mitochondrial electron transport chain (ETC) function can promote longevity. We performed an RNAi screen to probe the role of ETC components in modulating lifespan in the fruit fly Drosophila melanogaster. In this Research Perspective, we discuss our findings and how they may relate to similar studies in worms and mice.

摘要

衰老研究的一个主要目标是确定能延长远缘生物寿命的干预措施。近年来,对线虫和啮齿动物的基因研究表明,对线粒体电子传递链(ETC)功能重要的基因进行适度失活可延长寿命。我们进行了一项RNA干扰筛选,以探究ETC成分在调节果蝇寿命中的作用。在这篇“研究视角”文章中,我们讨论了我们的发现以及它们与在蠕虫和小鼠中进行的类似研究可能存在的关联。

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本文引用的文献

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Perturbation of mitochondrial complex V alters the response to dietary restriction in Drosophila.线粒体复合物 V 的扰动改变了果蝇对饮食限制的反应。
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Extension of Drosophila life span by RNAi of the mitochondrial respiratory chain.通过 RNAi 技术抑制线粒体呼吸链延长果蝇寿命。
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Deletion of the mitochondrial superoxide dismutase sod-2 extends lifespan in Caenorhabditis elegans.线粒体超氧化物歧化酶sod-2的缺失可延长秀丽隐杆线虫的寿命。
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Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans.针对衰老的氧化损伤理论:超氧化物歧化酶可抵御氧化应激,但对秀丽隐杆线虫的寿命几乎没有影响。
Genes Dev. 2008 Dec 1;22(23):3236-41. doi: 10.1101/gad.504808.
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Early mitochondrial dysfunction in long-lived Mclk1+/- mice.长寿的Mclk1+/-小鼠早期线粒体功能障碍。
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