Stem cell transplants have been of great interest to aging researchers, and, in a new study, they have successfully increased mouse lifespan by using stem cell therapy. While this has been previously achieved, this experiment was more refined than older studies and sheds new light on the potential of tissue regeneration through stem cells.

The significant extension of maximum lifespan could be considered an indication that any intervention is targeting a core hallmark of aging or, in the case of small increases of lifespan, at least indirectly influencing it.

Through bone marrow transplants, the researchers have significantly increased the lifespans of mice and believe that they are directly targeting an aging process directly [1]. Given that stem cell exhaustion is a hallmark of aging, they are likely correct.

Given the chance, there are very few of us who wouldn’t want to slow down the aging process. Chasing that fountain of youth is a major branch of medical science at the moment, and a hardy little worm known as C. elegans is probably the most prolific test subject. Now, a team at Scripps Research has found that blocking a particular enzyme can extend the lifespan of these worms by almost half again.

Today, we want to spotlight a new publication that charts the senescence-associated secretory phenotype (SASP), which consists of the various secreted signals given out by senescent cells during aging.

Senescent cells and the SASP

As we get older, an increasing number of our cells enter into a state known as senescence. They cease dividing and supporting the tissues and organs of which they are part and, instead, secrete a range of harmful chemical signals. This cocktail of harmful signals is known as the senescence-associated secretory phenotype (SASP).

Clinical trials to remove senescent cells have now begun.