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Autophagy regulation pathways comprise the network of signaling and molecular events that control the induction, progression, and termination of autophagy—the conserved cellular process where cytoplasmic constituents are sequestered in autophagosomes and degraded following lysosomal fusion. The most canonical regulators include mTOR (negative regulator) and AMPK (positive regulator), which signal through the ULK1 complex to control autophagy initiation. Downstream, proteins such as Beclin-1 and various ATGs coordinate autophagosome nucleation, elongation, maturation, and substrate selectivity. These pathways integrate environmental cues (e.g., nutrient levels, stress) and are pivotal for cell survival, quality control, and disease adaptation, linking autophagy to a wide spectrum of physiological and pathological states. In summary, "Autophagy regulation pathways" is not a discrete molecular drug target/receptor, but an umbrella term for a collection of signaling processes that coordinate autophagy and are modulated pharmacologically via distinct upstream nodes.
mTOR inhibition (de-represses autophagy initiation via ULK1 complex) AMPK activation (stimulates autophagy through ULK1 activation and mTOR inhibition) Lysosomal inhibition (blocks the completion phase of autophagy, causing autophagosome accumulation)
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