Autophagy (or autophagocytosis) (from the Ancient Greek αὐτόφαγοςautóphagos, meaning “self-devouring”[1] and κύτοςkýtos, meaning “hollow”[2]) is the natural, regulated mechanism of the cell that removes unnecessary or dysfunctional components.[3] It allows the orderly degradation and recycling of cellular components.[4][5]
Three forms of autophagy are commonly described:
macroautophagy,
microautophagy, and
chaperone-mediated autophagy (CMA). In macroautophagy, expendable
cytoplasmic constituents are targeted and isolated from the rest of the cell within a double-membraned
vesicle known as an autophagosome,[6][7] which, in time, fuses with an available lysosome, bringing its specialty process of waste management and disposal; and eventually the contents of the vesicle (now called an autolysosome) are degraded and recycled.
In disease, autophagy has been seen as an adaptive response to stress, promoting survival of the cell; but 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 in existence and frequently used from the middle of the 19th century[8]. In its present usage, the term autophagy was coined by Belgian biochemist Christian de Duve in 1963 based on his discovery of the functions of lysosome.[3] The identification of autophagy-related genes in yeast in the 1990s allowed researchers to deduce the mechanisms of autophagy,[9][10][11][12][13] which eventually led to the award of the 2016 Nobel Prize in Physiology or Medicine to Japanese researcher Yoshinori Ohsumi.[14]
Mandatory FDA Disclaimer: Not intended to diagnose, treat, cure or prevent any disease.
Mandatory FDA Disclaimer: Not intended to diagnose, treat, cure or prevent any disease.
