Senescence Deceleration is the clinical objective of slowing the rate at which cells and tissues enter the state of cellular senescence, a permanent state of cell cycle arrest that contributes significantly to aging and chronic disease. Senescent cells, often termed “zombie cells,” accumulate with age, secrete pro-inflammatory molecules (the Senescence-Associated Secretory Phenotype or SASP), and disrupt the function of surrounding healthy tissue. Deceleration protocols aim to reduce the burden of these dysfunctional cells and maintain a youthful proliferative capacity in healthy cells. This strategy is a core tenet of modern longevity medicine and anti-aging research.
Origin
The term combines senescence (from Latin senex ‘old man’ or ‘old age’), the biological process of cellular aging, with deceleration, implying a therapeutic slowing of this inevitable process. The concept is central to geroscience, which views aging as a modifiable risk factor for major chronic diseases. Clinical efforts are increasingly focused on intervening in this fundamental, molecular mechanism of aging.
Mechanism
Deceleration is achieved through interventions that reduce the accumulation of DNA damage and oxidative stress, the primary triggers for senescence induction. This may involve optimizing mitochondrial function and enhancing cellular repair mechanisms, such as autophagy and DNA repair pathways. Furthermore, targeted use of senolytic agents, which selectively induce apoptosis in senescent cells, is a key strategy to actively reduce the burden of the SASP and its associated systemic inflammation.
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