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Autophagy: A Critical Regulator of Cellular Metabolism and Homeostasis
Stefan W. Ryter,Suzanne M. Cloonan,Augustine M. K. Choi 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.1
Autophagy is a dynamic process by which cytosolic mate-rial, including organelles, proteins, and pathogens, are sequestered into membrane vesicles called autopha-gosomes, and then delivered to the lysosome for degra-dation. By recycling cellular components, this process provides a mechanism for adaptation to starvation. The regulation of autophagy by nutrient signals involves a com- plex network of proteins that include mammalian target of rapamycin, the class III phosphatidylinositol-3 kinase/Be-clin 1 complex, and two ubiquitin-like conjugation systems. Additionally, autophagy, which can be induced by multiple forms of chemical and physical stress, including endo-plasmic reticulum stress, and hypoxia, plays an integral role in the mammalian stress response. Recent studies indicate that, in addition to bulk assimilation of cytosol, autophagy may proceed through selective pathways that target distinct cargoes to autophagosomes. The principle homeostatic functions of autophagy include the selective clearance of aggregated protein to preserve proteostasis, and the selective removal of dysfunctional mitochondria (mitophagy). Additionally, autophagy plays a central role in innate and adaptive immunity, with diverse functions such as regulation of inflammatory responses, antigen presen-tation, and pathogen clearance. Autophagy can preserve cellular function in a wide variety of tissue injury and disease states, however, maladaptive or pro-pathogenic outcomes have also been described. Among the many diseases where autophagy may play a role in-clude proteo-pathies which involve aberrant accumulation of proteins (e.g., neurodegenerative disorders), infectious diseases, and metabolic disorders such as diabetes and metabolic syndrome. Targeting the autophagy pathway and its regu-latory components may eventually lead to the develop-ment of therapeutics.
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