Senescence Delay refers to interventions aimed at slowing or postponing the onset of cellular senescence, a state where cells cease dividing but remain metabolically active, secreting pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Postponing this accumulation is a primary target in extending health span, as senescent cells contribute significantly to chronic disease. This is a direct attempt to mitigate biological aging at the cellular level.
Origin
This terminology originates from the molecular biology of aging research, focusing specifically on modulating the mechanisms that drive cells into this irreversible state of arrested growth. It is distinct from merely extending lifespan; the focus is on maintaining youthful cellular function. The concept is highly relevant to understanding age-related hormonal shifts.
Mechanism
Strategies for delay often involve modulating pathways that control cell cycle checkpoints, such as p53 or p16 signaling, or employing senolytic agents that selectively clear existing senescent cells. Furthermore, optimizing mitochondrial health reduces the baseline oxidative stress that often triggers premature senescence entry. Supporting robust DNA repair mechanisms is also paramount to preventing the damage that initiates this non-proliferative state.
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