Figure 1

Both telomeric and non-telomeric DNA damage contribute to the stabilisation of cellular senescence. DNA damage at telomeres is distinct from that throughout the genome; it is irreparable due to the repression of DNA repair pathways by telomere bound proteins, known as the “shelterin” complex. This contributes to a permanent DNA damage response (DDR). However, continuous generation of short-lived DDR foci by elevated reactive oxygen species (ROS) may equally contribute to the maintenance of the phenotype, as long as a dynamic equilibrium between damage induction and repair can be maintained.