Fig. 1

Mechanism and effect of autophagy and apoptosis. Autophagy and apoptosis are two vital mechanisms for maintaining cellular homeostasis under stress conditions. Autophagy is an evolutionarily conserved cellular degradation process that is activated in response to cellular stress signals. The ULK1 complex mediates autophagy initiation, and phagocytic vacuole formation involves the class III phosphoinositide 3-kinase (PI3K) complex, comprising PI3K, ATG14L, Beclin 1, VPS34, and VPS15. The ATG5/ATG12/ATG16 complex and LC3II are subsequently involved, and during autophagosome formation, p62 binds to LC3II while the phagophore expands, encapsulating intracellular material to form autophagosomes. Lysosomes fuse with autophagosomes, providing hydrolytic enzymes for the degradation of phagocytosed material. Two signaling pathways for apoptosis exist: intrinsic and extrinsic. Various intracellular microenvironment perturbations such as DNA damage, growth factor deprivation, and oxidative stress activate the intrinsic apoptotic pathway. Mitochondrial outer membrane permeabilization (MOMP) is a critical step in apoptosis, leading to the release of intermembrane proteins such as cytochrome c. Proteins of the BCL family promote or inhibit this process. Cytochrome c binds to Apaf-1 to form apoptotic bodies, promoting caspase activation. In contrast, extrinsic apoptosis is triggered by the binding of death ligands (e.g., FasL, TNF-α) to death receptors (e.g., Fas, TNF-R), resulting in the assembly of death-inducing signaling complexes (DISC) and the activation of downstream effector caspases (e.g., caspases 3, 6, 7, 8, 10). The two play different roles at different stages