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Autophagy
Autophagy (or autophagocytosis) (from the Greek ''auto-'', "self" and ''phagein'', "to eat"), is the natural, destructive mechanism that disassembles, through a regulated process, unnecessary or dysfunctional cellular components.
Autophagy allows the orderly degradation and recycling of cellular components.〔 During this process, targeted cytoplasmic constituents are isolated from the rest of the cell within a double-membraned vesicle known as an autophagosome. The autophagosome then fuses with a lysosome and the contents are degraded and recycled.〔 〕 There are three different forms of autophagy that are commonly described, namely macroautophagy, microautophagy and chaperone-mediated autophagy. In the context of 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.
==Discovery and origin of the name==
The process of autophagy was observed by Keith R. Porter and his postdoctoral student Thomas Ashford at the Rockefeller Institute. In January 1962 they reported that there were an increased number of lysosomes in the liver cells of rat after addition of glucagon, and that some displaced lysosomes towards the centre of the cell contained other cell organelles such as mitochondria. This was the first reported evidence in the English literature of intracellular digestion of cell organelles (which they called autolysis after Christian de Duve). However Porter and Ashford wrongly interpreted their data as lysosomes being formed (ignoring the pre-existing organelles), lysosomes could not be cell organelles but part of cytoplasm such as mitochondria, and that hydrolytic enzymes were produced by microbodies. In early 1963, the American Journal of Pathology published a detailed ultrastructural description of "focal cytoplasmic degradation," which referenced a 1955 German study of injury-induced sequestration. Z. Hruban and colleagues recognized three continuous stages of maturation of the sequestered cytoplasm to lysosomes, and that the process was not limited to injury states, but also functioned under physiological conditions for "reutilization of cellular materials," and the "disposal of organelles" during differentiation. Inspired by this discovery, the term "autophagy" was invented by de Duve, the Nobel Prize-winning discoverer of lysosomes and peroxisomes. 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 postdoctoral student Russell L. Peter, he subsequently established that lysosomes are indeed responsible for glucagon-induced autophagy. This was the first time the fact that lysosomes are the sites of intracellular autophagy was established. He first publicly used the word at the first international symposium on lysosomes, the ''Ciba Foundation Symposium on Lysosomes'' held in London during 12–14 February 1963. He specifically introduced it while making a speech on "The Lysosome Concept" to explain the term "cytolysomes" introduced by Alex B. Novikoff.〔
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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