Life span heterogeneity is a hallmark of the ageing process. It is also a characteristic feature of telomere-dependent replicative senescence. We review here evidence showing that telomere shortening is heterogeneous between telomeres and between cells, and relate this to cell-to-cell variation in mitochondrial function and production of reactive oxygen species (ROS). Telomere shortening is to a large extent governed by ROS-mediated telomeric DNA damage, and we show here that apparently stochastic variation in mitochondrial ROS production can account for vast differences in replicative potential between individual cell lineages.
|Original language||English (US)|
|Title of host publication||Telomeres and Telomerase in Ageing, Disease, and Cancer|
|Subtitle of host publication||Molecular Mechanisms of Adult Stem Cell Ageing|
|Publisher||Springer Berlin Heidelberg|
|Number of pages||14|
|State||Published - Dec 1 2008|
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