Senescent cells accumulate with age, a situation that appears more a result of the aging immune system failing to achieve timely clearance of newly senescent cells rather than a significant increase in the pace at which cells become senescent. Senescence occurs in response to cellular damage and stress, but also when somatic cells reach the Hayflick limit on replication. A senescent cell becomes larger, ceases replication, and devotes its energies to the secretion of pro-growth, pro-inflammatory signals. In the short term and in youth this is usually beneficial, helping to coordinate tissue maintenance, regeneration, and suppression of potentially cancerous cells. When sustained for the long term, the signaling of senescent cells is disruptive to tissue structure and function, however, contributing to the damaging chronic inflammation of aging.
In principle, clearing out lingering senescent cells should improve the ability of other classes of rejuvenation therapy to produce benefits. This is particularly thought to be case for stem cell and exosome therapies that rely upon generating favorable signals to improve the behavior of a patient's cells, thereby dampening chronic inflammation and hopefully enhancing regeneration and tissue maintenance. Senescent cells and signaling therapies stand in opposition, and it makes sense that a reduced burden of senescent cells should improve outcomes for signaling therapies.
