Autophagy

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

Autophagy allows the orderly degradation and recycling of cellular components. In macroautophagy, targeted cytoplasmic constituents are isolated from the rest of the cell within a double-membraned vesicle known as an autophagosome. The autophagosome eventually fuses with lysosomes and the contents are degraded and recycled. Two additional forms of autophagy are also commonly described: 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. The identification of autophagy-related genes in yeast in the 1990s let researchers figure out the mechanisms of autophagy, and led to the award of the 2016 Nobel Prize in Physiology or Medicine to Japanese autophagy researcher Yoshinori Ohsumi.

Autophagy was first observed by Keith R. Porter and his student Thomas Ashford at the Rockefeller Institute. In January 1962 they reported an increased number of lysosomes in rat liver cells after addition of glucagon, and that some displaced lysosomes towards the centre of the cell contained other cell organelles such as . They called this autolysis after Christian de Duve and Alex B. Novikoff. However Porter and Ashford wrongly interpreted their data as lysosome formation (ignoring the pre-existing organelles). Lysosomes could not be cell organelles, but part of cytoplasm such as , and that hydrolytic enzymes were produced by microbodies. In 1963 researchers published a detailed ultrastructural description of "focal cytoplasmic degradation," which referenced a 1955 German study of injury-induced sequestration. The study recognized three continuous stages of maturation of the sequestered cytoplasm to lysosomes, and that the process was not limited to injury states that functioned under physiological conditions for "reutilization of cellular materials," and the "disposal of organelles" during differentiation. Inspired by this discovery, de Duve christened the phenomena "autophagy". Unlike Porter and Ashford, de Duve conceived the term as a part of lysosomal function while describing the role of glucagon as a major inducer of cell degradation in the liver. With his student Peter, he established that lysosomes are responsible for glucagon-induced autophagy. This was the first time the fact that lysosomes were established as the sites of intracellular autophagy.

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