Greaves Laura C, Turnbull Doug M
Mitochondrial Research Group, Institute for Ageing and Health, The Medical School, Newcastle University, Newcastle Upon Tyne, NE2 4HH, UK.
Biochim Biophys Acta. 2009 Oct;1790(10):1015-20. doi: 10.1016/j.bbagen.2009.04.018. Epub 2009 May 4.
The mechanism by which we age has sparked a huge number of theories, and is an area of intense debate. As the elderly population rises, the importance of elucidating these mechanisms is becoming more apparent as age is the single biggest risk factor for a number of diseases such as cancer, diabetes and neurodegenerative disease. Mitochondrial DNA (MtDNA) mutations have been shown to accumulate in cells and tissues during the ageing process; however the question as to whether these mutations have a causal role in the ageing process remains an area of uncertainty. Here we review the current literature, and discuss the evidence for and against a causal role of mtDNA mutations in ageing and in the pathogenesis of age-related disease.
我们衰老的机制引发了大量理论,并且是一个激烈争论的领域。随着老年人口的增加,阐明这些机制的重要性日益凸显,因为年龄是多种疾病(如癌症、糖尿病和神经退行性疾病)的单一最大风险因素。线粒体DNA(MtDNA)突变已被证明在衰老过程中会在细胞和组织中积累;然而,这些突变在衰老过程中是否具有因果作用仍是一个不确定的领域。在这里,我们回顾当前的文献,并讨论支持和反对mtDNA突变在衰老及与年龄相关疾病发病机制中具有因果作用的证据。