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【Nature】衰老的端粒/线粒体轴线
最近对端粒（染色体端部的保护性末端）和线粒体之间的一个功能联系的揭示，提出这样一个可能性：二者都可能涉及与衰老相关的过程。现在，对来自小鼠心脏和肝脏组织的造血干细胞的转录组（全部RNA内容）所做的一项分析，表明存在一个“端粒- p53-PGC”轴线，这个轴线将端粒功能丧失与器官功能降低联系了起来，而且也可能与跟年龄相关的病变联系了起来。在端粒丧失功能的小鼠中，p53-调控的细胞生长停滞被激活，接着它又抑制PGC-1α 和 PGC-1β（代谢过程和线粒体过程的主要调控因子）。这会导致线粒体质量减少、线粒体功能丧失和ATP生成量减少、糖生成受损、心肌功能受损和活性氧增加。
原文见附件
http://www.nature.com/nature/journal/v470/n7334/abs/nature09787.html
SQ2010AA0320490001.pdf (562.26k) 在线查看 本期Nature对上述论文给以很高的评价（见附件），认为这个发现有助于建立一个统一的衰老机制
Ageing is a complex process involving defects in various cellular components. The latest evidence suggests a unifying mechanism for cellular ageing that is relevant to the development of common age-related diseases.
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With age, telomere damage in the nucleus triggers the activation of p53, which can have different effects. In proliferative cells, p53 halts both cell growth and DNA replication, potentially causing apoptotic cell death. Sahin et al.1 report that p53 also represses the expression of PGC-1 in mitochondria, reducing the function and number of these organelles, and so leading to age-related dysfunction of mitochondrion-rich, quiescent tissues. The mitochondrial derangements driven by loss of PGC-1 activity may independently lower the threshold for the generation of toxic intermediates such as reactive oxygen species (ROS), which damage mitochondrial DNA, thus setting up a vicious cycle of further mitochondrial dysfunction.
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作者:admin@医学,生命科学 2011-02-17 11:03
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