Over at Ouroboros, some scientific speculation on the relationships between mitochondrial DNA (mtDNA) damage and aging that might - or might not - be illustrated by accelerated aging (or progeroid) conditions. Progeroid conditions are associated with failures of the repair processes for nuclear DNA, but how does the separate DNA in mitochondria figure in to this? "Repair mechanisms also exist for mitochondrial DNA, [but] do deficiencies in mtDNA repair play a similar role in aging? We've already seen that mitochondrial DNA damage accumulates with age. And calorie restriction, the gold standard of lifespan extension, prevents this increase in damage. ... The authors argue that the increased level of chromosomal breakage and the replicative pausing in the mutant mouse are responsible for the progeroid symptoms ... In their view, mitochondrial DNA replication is actually upregulated [so as to provide more energy] to compensate for the reduction in replication capacity. ... The phenotype of DNA repair mutants could be caused not by mutations themselves, but by the effort it takes to prevent DNA mutation from occurring past some threshold which would cause cellular catastrophe. ... Is it possible that the problem in progeroid models is not due to the DNA damage itself, but to [the energy-generation demands placed upon mitochondria in order] to prevent a catastrophic collapse of DNA integrity?"