The accumulation of cellular damage is a feature common to all aging cells and leads to a decreased ability of the organism to survive. The overall rate at which damage accumulates is influenced by conserved metabolic factors (longevity pathways and regulatory proteins), which control life span through adjusting mechanisms for maintenance and repair. Autophagy, the major catabolic process of eukaryotic cells, which has the capacity to degrade and recycle damaged macromolecules and organelles, is implicated in aging and in the incidence of diverse age-related pathologies. Recent evidence shows further that autophagic activity is required for life span extension in various long-lived mutant organisms, and that numerous autophagy-related genes or proteins serve as targets that longevity pathways regulate directly. These findings support the emerging view that autophagy acts as a central regulatory mechanism of aging in divergent eukaryotic species.
