| Promote induction of autophagy |
Lack of induction due to deficits in signaling or autophagic machinery Lack of induction due to defective recognition of damaged proteins/organelles Feedback inhibition of induction from chronic autophagic stress
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| Promote lysosomal function to prevent/alleviate autophagic stress |
Age- and disease-associated decline in lysosomal function Expansion of AV intermediates responsible for toxic species generation Prolonged sequestration of essential components, making them unavailable for recycling
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| Blunt or slow autophagy induction |
Autophagic stress due to high levels of induction Autophagic/degradative stress overwhelming the capacity of cell to recycle membranes or to synthesize/regenerate important cellular components Autophagy induced for cell death execution (will need to balance loss of irreplacable cell against benefit of ridding organism of defective cell)
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| Enhance degradation of specific cargo without increasing overall autophagic flux |
Critical components degraded through bystander effect as result of autophagy induced for other reasons Aggregate-prone proteins or damaged mitochondria in aging subject with less efficient biosynthetic capacity
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