Autophagy is a conserved cellular process whereby long-lived and aggregated proteins, as well as excess and damaged organelles are targeted by a double membrane vesicle or autophagosome for elimination. Basal autophagic activity is present in all cells and plays a homeostatic role, allowing the use of basic molecular components (amino acids) as building blocks or energy source.
Physiologically, autophagy plays critical roles during organismal development and immune response, by regulating growth and cooperating with the adaptive immune system. In disease states, such as neurodegenerative conditions, inefficient autophagic activity leads to the accumulation of abnormal proteins and formation of intracellular aggregates. Autophagy provides a mechanism to battle and eliminate infectious pathogens. In cancer, autophagy plays a role promoting or inhibiting tumor growth in a system and stage dependent manner.
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Macroautophagy: Cytosolic components are sequestered within a double membrane organelle or autophagosome. Fusion of autophagosomes with lysosomes forms the autolysosome, where degradation of cytosolic components occurs. Hereafter, macroautophagy is referred to as autophagy.
Microautophagy: Lysosomes directly engulf cytosolic components via lysosomal membrane invagination.
Chaperone-Mediated Autophagy: Chaperone proteins (e.g., heat shock cognate 70 protein; HSC-70) interact with cytosolic proteins destined for degradation. This complex is recognized by a lysosomal-associated membrane protein-2A (LAMP-2A), resulting in the translocation of the unfolded cytosolic protein into the lysosome.
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