Anti-Senescence Signalling denotes the complex network of intracellular communication pathways that actively inhibit cellular senescence, a state of irreversible growth arrest associated with aging and disease. This critical biological process involves modulating gene expression to maintain cellular vitality and prevent the accumulation of dysfunctional cells. Effectively managing these signals is central to promoting tissue integrity and extending healthspan. Clinical strategies targeting these pathways seek to delay age-related decline and bolster systemic resilience.
Origin
The term derives from the Greek and Latin roots anti (against) and senescere (to grow old), directly addressing the biological mechanisms of aging. Its scientific foundation lies in the discovery of cellular limits to replication, the Hayflick limit, and the subsequent identification of senescence-associated secretory phenotype (SASP). The study of longevity genes and their regulatory loops, such as sirtuins and mTOR, established the concept of modifiable anti-senescence pathways.
Mechanism
This signaling operates by activating specific molecular effectors, including sirtuins, AMPK, and components of the DNA repair machinery. These pathways collectively suppress the activity of pro-senescence transcription factors and mitigate oxidative stress. Furthermore, anti-senescence signaling promotes the clearance of senescent cells through processes like apoptosis or immunosurveillance. This continuous cellular maintenance is vital for preserving tissue function and preventing chronic, low-grade inflammation, a hallmark of aging.
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