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p66Shc、氧化应激与衰老:将寿命决定因素引入线粒体

p66Shc, oxidative stress and aging: importing a lifespan determinant into mitochondria.

作者信息

Pinton Paolo, Rizzuto Rosario

机构信息

Department of Experimental and Diagnostic Medicine, Section of General Pathology, ER-GenTech Laboratory and Interdisciplinary Center for the Study of Inflammation (ICSI), University of Ferrara, Ferrara, Italy.

出版信息

Cell Cycle. 2008 Feb 1;7(3):304-8. doi: 10.4161/cc.7.3.5360. Epub 2007 Nov 20.

Abstract

The 66 KDa isoform of Shc and its signalling properties have attracted in the past years major interest in aging research. Here, we summarize p66Shc functions and outline a specific signalling route leading to mitochondrial import, that accounts for its pro-apoptotic activity upon oxidative stress. This model, that could explain the alterations of mitochondrial Ca2+ homeostasis observed after oxidative stress, highlights novel pharmacological targets in age-related disorders.

摘要

过去几年,Shc的66千道尔顿同工型及其信号传导特性在衰老研究中引起了极大关注。在此,我们总结了p66Shc的功能,并概述了一条导致线粒体导入的特定信号通路,该通路解释了其在氧化应激时的促凋亡活性。这个模型可以解释氧化应激后观察到的线粒体钙稳态改变,突出了与年龄相关疾病中的新药物靶点。

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