作者: Thomas von Zglinicki , Alexander Bürkle , Thomas BL Kirkwood
DOI: 10.1016/S0531-5565(01)00111-5
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摘要: Ageing is highly complex, involving multiple mechanisms at different levels. Nevertheless, recent evidence suggests that several of the most important are linked via endogenous stress-induced DNA damage caused by reactive oxygen species (ROS). Understanding how such contributes to age-related changes requires we explain these relate each other and potentially interact. In this article, review contributions cellular through (i) role nuclear its repair mediated actions poly(ADP-ribose) polymerase-1, (ii) telomeric contribution telomere-driven cell senescence, (iii) accumulation mutations in mitochondrial DNA. We describe an integrative approach studying mechanisms, coupled with computational modelling, may be considerable importance resolving some complexity ageing.