You might recall that researchers have put forward evidence to suggest that telomere shortening is caused by accumulated damage to mitochondrial DNA - essentially collapsing two areas of intense interest for gerontologists down to one root cause, if confirmed. Back then, I said:
We know that mitochondrial damage is tied to aging via mechanisms such as the production of damaging free radicals such as ROS - and that some researchers are working on solutions, such as the ability to replace all mitochondrial DNA in the body via protofection. We also know that progressive telomere shortening is tied to aging and age-related disease, and a number of different groups are working on strategies to safely lengthen telomeres.
There is strong evidence to believe that "tied to aging" in this context means "contributes to aging as a cause." Remember that aging is no more than an accumulation of damage in biochemical systems; when we look at these changes that take place with aging, we are looking at damage. This paper offers the possibility that if we repair or prevent the progressive accumulation of mitochondrial degeneration and damage, then the telomeres will take care of themselves - if the results are replicated, of course.
Building on this, I see that researchers are now pulling the action of telomerase into the forming picture:
Telomerase is a ribonucleoprotein that counteracts telomere shortening and can immortalise human cells. There is also evidence for a telomere-independent survival function of telomerase. However, its mechanism is not understood.
We show here that TERT, the catalytic subunit of human telomerase, protects human fibroblasts against oxidative stress. While TERT maintains telomere length under standard conditions, telomeres under increased stress shorten as fast as in cells without active telomerase. This is because TERT is reversibly excluded from the nucleus under stress in a dose- and time-dependent manner.
Extranuclear telomerase colocalises with mitochondria. In TERT-overexpressing cells, [mitochondrial DNA] is protected, mitochondrial membrane potential is increased and mitochondrial superoxide production and cell peroxide levels are decreased, all indicating improved mitochondrial function and diminished retrograde response. We propose protection of mitochondria under mild stress as a novel function of TERT.
So, poorly functioning mitochondria lead to telomere shortening, and telomerase somehow improves mitochondrial function to prevent that shortening. This is in place of the more expected path of undoing ongoing telomere shortening by adding extra repeat sequences to the end of the telomeres - that being the better understood function of telomerase.
Damaged mitochondria are a fundamental root cause of age-related degeneration far above and beyond the matter of telomeres. If telomerase acts to improve the state of mitochondria, this might explain why telomere length correlates so well with general measures of health in the old. It might even be the case that, setting aside cancer for one moment, telomere length really isn't that important in comparison to your mitochondrial health.
This all cries out for more research - the prospect of reducing two thorny problems down to one in the development of medical technologies to repair and prevent aging is very welcome. Regardless of the outcome, efforts to repair mitochondrial damage will remain very important to our future health and longevity, and are presently greatly underfunded in comparison to that importance.