Abstract
Autophagy (self-eating) is a conserved catabolic homeostatic process required forcellular metabolic demands by removal of the damaged molecules and organelles and for alleviation of stress initiated by pathology and infection. By such actions, autophagy is essential for the prevention of aging, disease, and cancer. Genetic defects of autophagy genes lead to a host of developmental, metabolic, and pathological aberrations. Similarly, the age-induced decline in autophagy leads to the loss of cellular homeostatic control. Paradoxically, such a valuable mechanism is hijacked by diseases, during tumor progression and by senescence, presumably due to high levels of metabolic demand. Here, we review both the role of autophagy in preventing cellular decline in aging by fulfillment of cellular bioenergetic demands and its contribution to the maintenance of the senescent state and SASP by acting on energy and nutritional sensors and diverse signaling pathways.
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