人老化的理论得到统一：细胞核，线立体，和老化

线粒体 (mitochondria) 存在于大多数真核细胞内，是细胞生命能量ATP的制造来源，为细胞的新陈代谢提供充足能量，所以线粒体在科学界也有细胞“动力工厂”之称。人体衰老与线粒体关系密不可分。氧自由基 [reactive oxygen species (ROS)] 让线粒体受损并无法得到修复，最终导致细胞因能量下降而趋向衰亡，使人体细胞老化速度不断加剧。

另外一项老化的机制，与细胞核 (nucleus) 内承载遗传基因的染色体终端 (telomere) 消耗有关。染色体的终端随着细胞分裂的次数不断减短，减短到一定程度时，细胞便停止分裂。所以染色体终端的长度，可能就是生命的定时器，它告诉细胞什么时候该停止分裂了。

线粒体老化机制和细胞核老化机制之间的关系是怎样的呢？在最近一期的《自然》杂志中有新的研究进展。

 

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.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.

 

 

-  Daniel P. Kelly1. Cell biology: Ageing theories unified. Nature Year published: (2011)Published online 09 February 2011
 
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09896.html?WT.ec_id=NATURE-20110210