A little Friday science; telomerase - or rather its sub-unit, Telomerase Reverse Transcriptase (hTERT) - appears to influence the way and degree to which oxidative stress damages mitochondrial DNA (mtDNA), causing cells to die via apoptosis. If you remove the capability for hTERT to interact with mitochondria via a suitable mutation, you find this: "Cells carrying this mutated hTERT not only have significantly reduced levels of mtDNA damage following [induction of oxidative stress], but strikingly also do not shown any loss of viability or cell growth. ... nuclear-targeted hTERT, in the absence of mitochondrial localization, is associated with diminished mtDNA damage, increased cell survival and protection against cellular senescence." A number of groups are working on the technologies required to manipulate telomeres and telomerase - these tools will be most useful.

Link: http://hmg.oxfordjournals.org/cgi/content/abstract/ddl098v1