衰老与疾病中的线粒体DNA修复
Mitochondrial DNA repair in aging and disease.
作者信息
Druzhyna Nadiya M, Wilson Glenn L, LeDoux Susan P
机构信息
Department of Cell Biology and Neuroscience, University of South Alabama, 307 University Boulevard, Mobile, AL 36688, USA.
出版信息
Mech Ageing Dev. 2008 Jul-Aug;129(7-8):383-90. doi: 10.1016/j.mad.2008.03.002. Epub 2008 Mar 13.
Mitochondria are organelles which, according to the endosymbiosis theory, evolved from purpurbacteria approximately 1.5 billion years ago. One of the unique features of mitochondria is that they have their own genome. Mitochondria replicate and transcribe their DNA semiautonomously. Like nuclear DNA, mitochondrial DNA (mtDNA) is constantly exposed to DNA damaging agents. Regarding the repair of mtDNA, the prevailing concept for many years was that mtDNA molecules suffering an excess of damage would simply be degraded to be replaced by newly generated successors copied from undamaged genomes. However, evidence now clearly shows that mitochondria contain the machinery to repair the damage to their genomes caused by certain endogenous or exogenous damaging agents. The link between mtDNA damage and repair to aging, neurodegeneration, and carcinogenesis-associated processes is the subject of this review.
线粒体是一种细胞器，根据内共生理论，它大约在15亿年前从紫色细菌进化而来。线粒体的一个独特特征是它们有自己的基因组。线粒体半自主地复制和转录其DNA。与核DNA一样，线粒体DNA（mtDNA）不断暴露于DNA损伤剂。关于mtDNA的修复，多年来流行的概念是，遭受过多损伤的mtDNA分子会简单地被降解，由从未受损基因组复制的新生成的后继分子所取代。然而，现在有证据清楚地表明，线粒体含有修复由某些内源性或外源性损伤剂对其基因组造成损伤的机制。mtDNA损伤与修复与衰老、神经退行性变和癌症相关过程之间的联系是本综述的主题。
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