Autophagy is the natural, regulated, destructive mechanism of the cell that disassembles unnecessary or dysfunctional components, involving in protein degradation, organelle turnover, and non-selective breakdown of cytoplasmic components. Generally speaking, autophagy exists three types, including macroautophagy, microautophagy, and chaperone-mediated autophagy, but the term "autophagy" usually indicates macroautophagy unless otherwise specified.
Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Despite its simplicity, recent progress has demonstrated that autophagy plays a wide variety of physiological and pathophysiological roles, which are sometimes complex.
Autophagy consists of several sequential steps—sequestration, transport to lysosomes, degradation, and utilization of degradation products—and each step may exert different function.
This progress initiates with production of the autophagosome, a double-membrane intracellular structure of reticular origin that engulfs cytoplasmic contents and ultimately fuses with lysosomes for cargo degradation.
In mammals, amino acid sensing and additional signals such as growth factors and reactive oxygen species regulate the activity of the protein kinases mTOR and AMPK. These two kinases regulate autophagy pathway through inhibitory phosphorylation of the Unc-51-like kinases ULK1 and ULK2. Induction of autophagy results in the dephosphorylation and activation of the ULK kinases. Autophagy is upregulated in response to extra- or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection.
Defective autophagy plays a significant role in human pathologies, including cancer, neurodegeneration, and infectious diseases. If you want to know more information about autophagy including definition, types, pathway and related diseases, you can click the following link: https://www.cusabio.com/c-20666.html.
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