These are the conserved signaling cascades that modulate cellular senescence, DNA repair mechanisms, and epigenetic drift, influencing the rate of physiological decline. These involve complex interactions related to sirtuins, mTOR, and AMPK, which are central to longevity science in endocrinology. Understanding these allows for targeted intervention to support robust cellular function over time.
Origin
The concept originates from molecular gerontology, where researchers identified conserved signaling networks across species that govern lifespan and healthspan. Clinically, this framework helps contextualize age-related endocrine shifts and cellular degradation observed in human physiology. It represents a modern shift from treating symptoms to addressing fundamental biological drivers of aging.
Mechanism
These pathways function by sensing nutrient availability and cellular stress, subsequently regulating mitochondrial biogenesis and proteostasis within the cell. For instance, caloric restriction mimetics often target these systems to induce beneficial cellular turnover processes. Successful modulation aims to enhance cellular resilience against cumulative molecular damage, thereby preserving endocrine and physiological integrity.
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