A collective term for the specific, highly conserved biochemical and molecular signaling cascades within cells that directly regulate lifespan, cellular resilience, and the organism’s adaptive response to stress and nutrient availability. These pathways include key regulators such as the sirtuins, mTOR, AMPK, and the insulin/IGF-1 axis, which function as central nodes governing the pace of aging and the capacity for tissue repair. Optimization of these pathways is a cornerstone of modern longevity intervention.
Origin
This concept stems directly from seminal research in model organisms like yeast, worms, and flies, which identified a small number of genetic mutations that dramatically extended lifespan, subsequently revealing the underlying biochemical pathways. The term represents the clinical synthesis of these evolutionary conserved mechanisms, applying findings from basic biology to human healthspan optimization. It marks the transition from descriptive aging research to targeted molecular intervention.
Mechanism
These pathways operate as cellular sensors, translating environmental cues—like nutrient abundance, energy status, and oxidative stress—into regulatory signals that modulate gene expression and protein activity. For example, nutrient restriction activates AMPK and sirtuins, which promote cellular maintenance and DNA repair, while nutrient excess activates mTOR and IGF-1 signaling, favoring growth and proliferation. By precisely modulating the activity of these pathways, clinicians can encourage a cellular state biased toward resilience and long-term survival.
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