Cellular autophagy pathway

Cellular autophagy pathways comprise a set of conserved intracellular degradation systems by which eukaryotic cells sequester cytosolic components—including damaged proteins, dysfunctional organelles, and invading pathogens—into double-membrane vesicles called autophagosomes, which subsequently fuse with lysosomes for cargo breakdown and recycling[1][2][3][5][7][9]. The main forms of autophagy in mammals are *macroautophagy* (the classical pathway), *microautophagy* (direct lysosomal engulfment), and *chaperone-mediated autophagy* (selective protein targeting via chaperone recognition)[2][3][5]. The machinery involves numerous autophagy-related (ATG) proteins orchestrating initiation, nucleation, expansion, cargo selection, autophagosome maturation, and lysosomal fusion[1][5][7][9]. Autophagy is crucial for cellular homeostasis, stress adaptation, immune defense, and regulated cell death, and its dysregulation is implicated in cancer, neurodegeneration, infection, inflammation, and metabolic disease[4][6].

Other names

Autophagy pathwayCellular autophagyAutophagy

mTOR inhibitors (e.g., rapamycin) induce autophagy by inhibiting mTOR, releasing its suppressive effect on autophagy initiation PI3K inhibitors (such as 3-MA) inhibit autophagy nucleation Chloroquine/hydroxychloroquine inhibits late-stage autophagy by impairing lysosomal acidification and fusion Various experimental compounds (e.g., ULK1 inhibitors, Beclin-1 modulators)[9]