Abstract
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 |
| Pages | 43-56 |
| Number of pages | 14 |
| ISBN (Print) | 9783540737087 |
| DOIs | |
| State | Published - Dec 1 2008 |
ASJC Scopus subject areas
- Medicine(all)
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Cite this
Passos, J. F., Nelson, G., & Von Zglinicki, T. (2008). Telomeres, senescence, oxidative stress, and heterogeneity. In Telomeres and Telomerase in Ageing, Disease, and Cancer: Molecular Mechanisms of Adult Stem Cell Ageing (pp. 43-56). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-540-73709-4_3