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The autophagy-mitophagy pathway represents a set of evolutionarily conserved cellular processes that maintain internal homeostasis by degrading and recycling damaged organelles, misfolded proteins, and invasive pathogens, primarily via lysosomal degradation. General autophagy engulfs cytoplasmic contents in autophagosomes that fuse with lysosomes to enable degradation, whereas mitophagy is the selective elimination of defective mitochondria. Key molecules in these pathways include ULK1 complex, ATG proteins, PINK1, and Parkin. These pathways are implicated in major diseases such as neurodegeneration, cancer, and metabolic syndromes, and can be pharmacologically modulated, but are not themselves a therapeutic target in the sense of a single protein, receptor, or enzyme.
mTOR inhibition (induces autophagy); AMPK activation (induces autophagy/mitophagy); Lysosome acidification inhibition (blocks autophagic flux); Enhancement or suppression of specific autophagy/mitophagy regulators (e.g., PINK1, Parkin)
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