Trifunovic Aleksandra
Division of Metabolic Diseases, Department of Laboratory Medicine, Karolinska Institute, NOVUM, SE-14186 Stockholm, Sweden.
Biochim Biophys Acta. 2006 May-Jun;1757(5-6):611-7. doi: 10.1016/j.bbabio.2006.03.003. Epub 2006 Mar 31.
The accumulation of mitochondrial DNA mutations has been proposed as a potential mechanism in the physiological processes of ageing and age-related disease. Although mitochondria have long been anticipated as a perpetrator of ageing, there was little experimental evidence to link these changes directly with the cellular pathology of ageing. Recently, considerable progress in understanding basic mitochondrial genetics and in identifying acquired mtDNA mutations in ageing has been made. Furthermore, the creation of mtDNA-mutator mice has provided the first direct evidence that accelerating the mtDNA mutation rate can result in premature ageing, consistent with the view that loss of mitochondrial function is a major causal factor in ageing. This review will, therefore, focus on recent developments in ageing research related to the role played by mtDNA.
线粒体DNA突变的积累被认为是衰老和与年龄相关疾病生理过程中的一种潜在机制。尽管长期以来人们一直预期线粒体是衰老的元凶，但几乎没有实验证据将这些变化与衰老的细胞病理学直接联系起来。最近，在理解基本线粒体遗传学以及识别衰老过程中获得性mtDNA突变方面取得了相当大的进展。此外，mtDNA突变小鼠的产生提供了首个直接证据，表明加速mtDNA突变率可导致早衰，这与线粒体功能丧失是衰老的主要因果因素这一观点一致。因此，本综述将聚焦于与mtDNA作用相关的衰老研究的最新进展。
