Today is my birthday and to be coherent, I’m going to talk about cellular senescence, which is a cellular process strongly linked to aging.
Senescence is a cellular program where cells lose their ability to divide. Cell aging is not measured in hours or days, but in cell divisions – what is known as the Hayflick limit –. For human somatic cells this limit is ~40-60 divisions. Senescent cells stop dividing to prevent the multiplication and spread of dangerous elements. Thus, it plays an important preventive role by eliminating, for example, pre-cancerous cells. In addition, Senescent cells secrete inflammatory compounds that have effects both in themselves and in the surrounding tissues. These inflammatory effects are as important in tissue repair as in healing. But a continuous inflammation leads to disorganization and tissue destruction. Therefore, senescence per se is neither good nor bad, it all depends on its context and regulation.
Today we know that senescence is linked to telomeres shortening. Telomeres are 6 nucleotide sequences that are located at the ends of the chromosomes and are repeated hundreds of times (for vertebrates the sequence is (TTAGGG)n). Its function is to protect DNA from potential degradation and aberrant recombination. During each somatic cell division, the telomeres are shortened, because when the DNA is replicated, the ends are not copied.
Recent studies – done in mice – have shown that when senescent cells are eliminated, mice have an increased physical activity and motility, a reduction of aging symptoms and extended lifespan. This suggests that – in mice at least – aging is partly due to an accumulation of senescent cells (Baker et al., 2016 and Baar et al., 2017). If these observations are confirmed, treatments can be developed to improve the quality life for seniors. Good news when you are getting older!
