A number of research programs in recent years have pointed to an increased level of retrotransposon activity with aging. Retrotransposons are DNA sequences that can copy themselves to different locations in the genome, a parasitic addition that originated deep in evolutionary history. Retrotransposons are normally suppressed in youth, but increased retrotransposon activity occurs in later life, and is thought to bring disarray to cellular function. As is the case for most observed aspects of aging, there is plenty of room to debate just where retrotransposon activity sits in the complex web of cause and consequence.
Researchers here note that one class of retrotransposons escapes suppression in senescent cells, and this increased activity is important to the senescence-associated secretory phenotype (SASP) by which lingering senescent cells cause great harm to surrounding tissues. The SASP is highly inflammatory, and chronic inflammation is responsible for much of the downstream harms of aging. Removing senescent cells is the present preferred approach to building rejuvenation therapies capable of turning back age-related inflammation, but a sizable contingent of researchers are nonetheless interested in finding ways to dial down the SASP. This seems a more challenging task, one that will proceed increment by increment, as
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