Biological Aging Pathways are the fundamental, interconnected molecular and cellular processes that progressively lead to the decline in physiological function, increased susceptibility to disease, and loss of homeostatic capacity over time. These pathways represent the quantifiable mechanisms, such as telomere attrition, mitochondrial dysfunction, and cellular senescence, that drive the discrepancy between chronological age and functional biological age. Understanding these pathways is central to longevity medicine and clinical intervention.
Origin
The concept stems from decades of research in gerontology and molecular biology, culminating in the identification of key “hallmarks of aging” that are conserved across species. In the context of endocrinology, the focus emerged from observing how age-related hormonal declines, such as somatopause and andropause, directly interact with and accelerate these cellular degradation processes. The pathways provide a framework for therapeutic targeting of the aging process itself.
Mechanism
These pathways operate through a complex network of genetic and epigenetic regulators that govern cellular repair and metabolism. For instance, chronic low-grade inflammation, or inflammaging, is driven by senescent cells accumulating and releasing pro-inflammatory cytokines, which in turn disrupt hormonal signaling cascades. Furthermore, the insulin and IGF-1 signaling pathway is a master regulator; its over-activation can accelerate aging, while strategic modulation can promote cellular resilience and longevity through improved stress response mechanisms.
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