Autofagian

Autofagian, commonly known in English as autophagy, is a highly conserved catabolic process by which cells degrade and recycle cytoplasmic components through lysosomes. The term describes self-digestion to maintain cellular quality control, adapt to nutrient stress, and support development and immune responses.

Process: Initiation involves signaling pathways that sense nutrient status (e.g., mTORC1 inhibition) leading to activation of the ULK1 kinase complex. Nucleation and expansion form a double-membrane autophagosome, enclosing cytoplasmic cargo, including organelles and protein aggregates. The autophagosome then fuses with a lysosome to form an autolysosome, where lysosomal enzymes degrade the contents. The resulting macromolecules are recycled to support metabolism.

Types: Macroautophagy (the most studied form) involves sequestration of large portions of cytoplasm. Microautophagy directly engulfs cytosol by lysosomal invagination. Chaperone-mediated autophagy uses chaperone proteins to deliver specific soluble proteins to lysosomes.

Selective autophagy targets specific substrates, such as damaged mitochondria (mitophagy), peroxisomes (pexophagy), lipids (lipophagy), and pathogens (xenophagy).

Regulation and significance: Autophagy is tightly regulated by nutrient signals, energy status, and stress. It plays roles in development, immunity, and disease. Dysregulation is implicated in cancer, neurodegeneration, infections, and aging. Nobel Prize in Physiology or Medicine (2016) awarded to Yoshinori Ohsumi for discoveries related to the mechanisms of autophagy.

Terminology: In some languages, the process is referred to as autofagian; in scientific literature, autophagy is the common term.