Telomeres are caps of repeated DNA sequences at the end of chromosomes. A little telomere length is lost every time a cell divides and its DNA is replicated, and this is one portion of the limiting mechanism that causes the somatic cells that make up the overwhelming majority of tissues to divide only a set number of times and then destroy themselves. Stem cells on the other hand make use of the enzyme telomerase to add repeated DNA sections to the ends of their telomeres as needed. They must maintain lengthy telomeres as it is their job is to continually spin off new long-telomere somatic cells to keep tissues running smoothly. This is a considerable simplification of the actual situation, but it is good enough for this discussion. The important point here is that if you measure average telomere length in a given tissue, and immune cells from blood are the most commonly used for this purpose at the moment, what you are in fact measuring is a some combination of present cell replication rates, cell replenishment rates, and telomerase activity.
There is a statistically significant correlation between average telomere lengths in immune cells and age and illness across a population. This isn't so useful for any given individual looking at a number and trying to figure out whether or not it means anything for future health, but it is true that the older and more ill a person is, the more likely it is for average telomere length in immune cells to be comparatively short. Is this meaningful to efforts to extend life? That is a question worth asking twice, given that telomere length measures look very much like a secondary marker resulting from the characteristic decline of stem cell activity and tissue maintenance with advancing age, and we really want to aim at primary causes rather then secondary and later mechanisms.
Nonetheless, a fair number of researchers are interested in trying to lengthen telomeres as a potential way to treat illness or lengthen life, and in recent years one research group has used gene therapy to raise levels of telomerase in mice. This turns out to extend mouse life span, with the caveats that (a) short-lived mammals like mice actually have quite different telomere dynamics from long-lived mammals such as we humans, so it is far from clear as to what the same thing would do in people, and (b) it is by no means certain what exactly is going on under the hood here. Is telomerase keeping somatic cells alive for longer, it is increasing stem cell activity, is it perhaps interacting with mitochondria in some way to reduce their contribution to aging, or is some other as yet undiscovered mechanism is at work?
Researchers will come to a conclusion at some point, as there seems to be slow but steady progress towards further investigations of telomerase gene therapy in mice. The same group that pioneered this approach is now heading down the traditional path of attempts to apply this treatment as a late stage intervention for age-related disease and dysfunction. They do this because it is still the only practical way to bring treatments to the clinic these days: approaches are inevitably sidelined into marginal applications intended to be applied after the damage is done. It is a ridiculous situation, and one that causes immense damage to the pace of progress by diverting researchers away from producing methods of prevention.
The enzyme telomerase repairs cell damage produced by ageing, and has been used successfully in therapies to lengthen the life of mice. Now it has been observed that it could also be used to cure illnesses related to the ageing process. Researchers at the Spanish National Cancer Research Centre (CNIO) have for the first time treated myocardial infarction with telomerase by designing a very innovative strategy: a gene therapy that reactivates the telomerase gene only in the heart of adult mice, thus increasing survival rates in those animals by 17% following a heart attack.
"We have discovered that following a myocardial infarction, hearts that express telomerase show less heart dilatation, better ventricular function and smaller scars from the heart attack; these cardiac events are associated with an increased survival of 17% compared to control animals." Furthermore, everything points to cardiomyocytes - the cells responsible for heart beating - being regenerated in those hearts with telomerase, a long searched-for goal in post-heart-attack therapy. The regeneration of heart muscle would counter the formation of scars as a consequence of the heart attack, a tough tissue that hinders cardiac function and increases the likelihood of heart failure.
Coronary heart disease is one of the main causes of death in the developed world, and treatment success remains modest, with high mortality rates within 1 year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases, including heart disease. Here we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared with controls. Our work suggests telomerase activation could be a therapeutic strategy to prevent heart failure after MI.