Autophagy (literally “self-eating”) is a highly conserved eukaryotic cellular recycling process which is achieved through the coordination of different autophagy-related genes (ATGs). Through the degradation of cytoplasmic organelles, proteins, and macromolecules, and the recycling of the breakdown products, autophagy plays important roles in cell survival and maintenance. 

All living organisms undergo continous renovation. The cellular renovation requires synthesis of new components but also degradation of pre-existing materials,which can serve as building blocks. Eukaryotic cells have two major degradation systems, the lysosome and the proteasome. Proteasomal degradation has high selectivity, the proteasome generally recognizes only ubiquitinated substrates, which are primarily short-lived protiens. By contrast, degradation in lysosome does not follow such a simple pattern. Various cytoplasmic constituents, including organelles, aggregated proteins, and long-lived proteins are sequestered into double-membrane autophagosomes, which subsequently fuse with lysosomes where their contents are degraded.

Autophagic activity is critical to the maintenance of cellular homeostasis and energy balance. Autophagy is also a major protective mechanism, which allows cell survival in response to multiple stress conditions, such as nutrient or growth factor deprivation, hypoxia, reactive oxygen species (ROS), DNA damage, or intracellular pathogens.

Increasingly evidence has connected malfunctions in autophagic processes to many clinically relevant diseases including cancer, neurodegeneration, diabetes, autoimmunity, and cardiovascular disease. Development of autophagy-targeting therapies will depend on a deeper understanding of the benefits, and potential consequences, of altering autophagic activity.