Aging cells send out different signals depending on their origin
Not all aged cells are the same. A new study shows that the reason a cell stops dividing determines which signaling molecules it sends into its surroundings.
When cells age and stop dividing, they become senescent. They then secrete a cocktail of signaling molecules known as the SASP (senescence-associated secretory phenotype), the signaling profile of aged cells. For years, this SASP was considered more or less uniform. But new research shows that its composition varies depending on how the cell entered the senescent state.
Researchers compared cells that became senescent through activation of a cancer gene with cells that stopped dividing because the protein p16 was expressed. The study, published in the journal Aging, demonstrated that both groups of cells produce a different SASP profile. This means that the type of senescent cell determines the effects on surrounding tissue.
Which cell causes which damage?
This distinction has practical relevance. Senescent cells are associated with chronic inflammation, tissue breakdown, and an increased cancer risk. But if multiple types of SASP exist, the harmful effects may also differ by type. A treatment aimed at removing or neutralizing senescent cells, an approach being studied in the field, might affect one type differently than another.
Implications for aging research
This research refines the picture of cellular aging. It suggests that future studies should ask not only how many senescent cells are present, but also what type. Whether this distinction can be exploited therapeutically in humans is an open question. The findings are preliminary and were obtained in cultured cells, making follow-up studies in living organisms necessary.
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