Targeted clinical strategies designed to selectively eliminate senescent cells—those that have ceased dividing but remain metabolically active and secrete pro-inflammatory factors (SASP). Removing these cells is hypothesized to reverse aspects of age-related tissue dysfunction.
Origin
This is a relatively new field in aging research, stemming from the discovery of the SASP phenotype and the development of senolytic compounds capable of inducing apoptosis in these persistent cells. It directly addresses a key driver of inflammaging.
Mechanism
Strategies employ senolytic agents that exploit the differential survival pathways between healthy and senescent cells, often targeting the BCL-2 family or p53 pathways. In the context of hormonal health, reducing the chronic inflammatory burden released by senescent cells can restore local tissue sensitivity to circulating hormones.
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