Telomere shortening, a primary factor in the self-amplifying cycle between mitochondrial and telomeric DNA damage during cellular senescence, primarily causes telomere decapping . During cell division, the "end replication problem" shortens telomeres, causing the accumulation of single-strand breaks due to damage from ROS generated as a byproduct of mitochondrial respiration . It has also observed telomere dysfunction-induced foci (TIFs) in aged cells with elevated mitochondrial superoxide production, indicating telomere damage .