Molecular Aging Mechanisms encompass the fundamental, cellular-level processes that drive biological senescence, tissue dysfunction, and the accumulation of damage over time, ultimately leading to age-related disease. These mechanisms include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and altered intercellular communication. Understanding these core pathways is essential for developing targeted interventions aimed at extending healthspan.
Origin
This term is the foundation of modern biogerontology and longevity research, consolidating decades of findings from genetics, cell biology, and biochemistry into a unified theory of aging. It moves the focus from macroscopic organ failure to the microscopic processes of damage accumulation. The clinical application involves assessing and modulating these pathways to slow the intrinsic rate of cellular decline.
Mechanism
Each mechanism represents a failure in a critical maintenance pathway. For example, mitochondrial dysfunction leads to decreased ATP production and increased reactive oxygen species (ROS), contributing to oxidative stress and cellular damage. Epigenetic alterations disrupt gene expression patterns, causing cells to lose their youthful functional identity. Interventions are designed to restore mitochondrial function, activate sirtuins and AMPK pathways, and clear senescent cells, thereby directly counteracting these underlying molecular drivers of aging.
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