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Autophagy (or autophagocytosis) (from the Ancient Greek αὐτόφαγος autóphagos, meaning “self-devouring”[1] and κύτος kýtos, meaning “hollow”[2]) is the natural, regulated, destructive mechanism of the cell that disassembles unnecessary or dysfunctional components.[3]

Autophagy allows the orderly degradation and recycling of cellular components.[4][5] In macroautophagy, targeted cytoplasmic constituents are isolated from the rest of the cell within a double-membraned vesicle known as an autophagosome.[6][7] The autophagosome eventually fuses with lysosomes and the contents are degraded and recycled. Three forms of autophagy are commonly described: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). In disease, autophagy has been seen as an adaptive response to stress, which promotes survival, whereas in other cases it appears to promote cell death and morbidity. In the extreme case of starvation, the breakdown of cellular components promotes cellular survival by maintaining cellular energy levels.

The name “autophagy” was coined by Belgian biochemist Christian de Duve in 1963.[3] The identification of autophagy-related genes in yeast in the 1990s let researchers figure out the mechanisms of autophagy,[8][9][10][11][12] and led to the award of the 2016 Nobel Prize in Physiology or Medicine to Japanese autophagy researcher Yoshinori Ohsumi.[13]

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