Why telomeres shorten and restoration strategies in aging.
Telomeres are DNA repeats found at the ends of chromosomes. They serve to maintain chromosomal stability. The caveat is that they shorten each time the cell divides due the end replication problem.
That is, unless the cell expresses telomerase. Telomerase is a ribonucleoprotein complex (a complex containing protein and RNA) that can add back telomeric repeats.
So what happens if telomerase isn’t expressed? Well, after ~50 divisions the shortened telomeres induce a cellular state known as replicative senescence. Basically, the cell stops dividing. This is thought to be beneficial since it acts as a tumour protective mechanism by preventing uncontrolled cells from replicating too many times. However, it can also reduce the regenerative potential of tissues.
Senescent cells accumulate with age. Moreover, a weak negative correlation is also seen between age and telomere length.
For these reasons there is much interest in using telomere restoration strategies to target aging and for treatments people suffering with telomeropathies. But how would this be achieved and would it pose a cancer risk?
In this video we will address these questions and provide the details of why telomeres shorten with age and how the length could be restored.
Intrigued by the exciting and developing senotherapeutics field? Our market intelligence report on senotherapeutics (which target senescence) is now available – order your copy here and watch out for more senotherapeutics-related articles coming soon.
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