You might recall that it was back in 2007 I first mentioned research into links between age-related changes in mitochondria, the power plants of the cell, and telomeres, the structures at the end of your chromosomes that form a counter for cell state. Your cell is a complex, unified machine, so in many ways its not surprising to find links between portions of the clockwork that are known to be important in aging. You should wander back into the archives and refresh your memory:
We know that mitochondrial damage is tied to aging via mechanisms such as the production of damaging free radicals such as [reactive oxygen species] - 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 progessive 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.
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.
As I said back then, this cries out for more research - which seems to be taking place. A recent paper pulls the antioxidant catalase into the mix:
We used cultured mouse embryonic fibroblasts (MEF) isolated from mice lacking telomerase activity (Terc(-/-)) to analyze the redox balance and the functional consequences promoted by telomerase deficiency.
6-month-old Terc(-/-) [mice] showed higher oxidant capacity, lower catalase activity, greater oxidative damage, and higher TGF-beta1 and fibronectin levels ... In summary, telomerase deficiency reduces catalase activity, determining a redox imbalance that promotes overexpression of TGF-beta1 and extracellular matrix proteins.
Back a few years, researchers demonstrated that pouring extra catalase onto the mitochondria - via a genetic mutation to target the chemical to where it was needed - extends healthy life span. Catalase soaks up some fraction of damaging free radicals before they can degrade the mitochondria that produce them, and slowing mitochondrial damage is very beneficial to health and longevity. Is catalase level the mechanism by which telomerase helps out the mitochondria? Stay tuned: the more we know, the easier it will be to develop repair technologies that can set things back to the way they were when we were young.