autophagy
Definition
Autophagy is a highly conserved cellular degradation process where cells break down and recycle their own components through lysosomal machinery. This self-eating mechanism involves the formation of double-membrane vesicles called autophagosomes that engulf cytoplasmic material, damaged organelles, or protein aggregates, then fuse with lysosomes for degradation. Autophagy serves critical roles in cellular homeostasis, stress response, quality control, and survival during nutrient deprivation. Dysregulated autophagy is implicated in numerous diseases including cancer, neurodegenerative disorders, infectious diseases, and metabolic syndromes. The process is tightly regulated by autophagy-related genes (ATG genes) and signaling pathways including mTOR, AMPK, and ULK1 complexes, making it a crucial therapeutic target.
Visualize autophagy in Nodes Bio
Researchers can map autophagy regulatory networks by connecting ATG genes, upstream signaling molecules (mTOR, AMPK, PI3K), and downstream effectors. Network visualization reveals how autophagy intersects with apoptosis, inflammation, and metabolic pathways. Users can overlay drug targets, disease associations, or expression data to identify intervention points and understand how autophagy modulation affects broader cellular networks in specific disease contexts.
Visualization Ideas:
- ATG gene regulatory networks showing transcriptional and post-translational control
- Autophagy-apoptosis crosstalk networks illustrating cell fate decisions
- Disease-specific autophagy dysfunction maps connecting genetic variants to phenotypes
Example Use Case
A pharmaceutical team investigating autophagy modulators for Alzheimer's disease uses network analysis to map connections between autophagy genes (BECN1, ATG5, ATG7) and amyloid-beta clearance pathways. By visualizing interactions between autophagy machinery, tau protein networks, and neuroinflammatory responses, they identify that enhancing autophagy through TFEB activation not only promotes protein aggregate clearance but also modulates microglial activation. This network perspective reveals combination therapy opportunities targeting both autophagy induction and inflammation simultaneously.