Autophagy is a highly conserved process by which intracellular contents are engulfed and self-consumed by de-novo formed autophagosomes. These double- or multi-membrane enclosed vesicles, formed de novo, surround portions of cytosol, including organelles such as mitochondria and endoplasmic reticulum (ER). The mature autophagosome eventually fuses with the lysosome, forming an autolysosome, in which its contents are degraded by lysosomal enzymes. Autophagy is a mechanism by which the cell recycles cellular building blocks and nutrients, scavenges damaged organelles and aggregated, misfolded proteins, and disposes of intracellular pathogens. As such, the autophagic process plays a critical role in maintaining cellular homeostasis, and especially contributes to cell survival during times of stress. Autophagy is often observed during programmed cell death, where it may serve to either prevent further damage and counter the death stimulus, or may actually facilitate cell death by excessive self-consumption. At the molecular level, a group of Atg genes, originally identified in yeast, mediate the induction, nucleation, and elongation of the autophagosome membrane. Several signaling pathways, including those that sense growth factors, nutrient and energy availability, converge on the mTOR kinase, a central regulator of autophagy induction.
