Autophagy is a collection of self-degradative processes in which cells remove dysfunctional or unnecessary components via a mechanism dependent on lysosomes, allowing cellular materials recycling and orderly degradation. Autophagy is important for the homeostasis of energy in normal development and in response to nutrient stress. Autophagy also serves as a major quality control guardian in eliminating aggregated and misfolded proteins, removing damaged organelles (e.g., mitochondria, peroxisomes, and endoplasmic reticulum), and clearing intracellular pathogens. Autophagy exerts multiple functions in a broad spectrum of biological activities, including nutrient starvation, meiosis, repair mechanisms, programmed cell death, and infection. Besides, autophagy also participates in immune responses. For example, in immunosurveillance in dendritic cells mediated by MHC class II molecules, autophagy is demonstrated to be responsible for feeding endogenous proteins to endosomal/lysosomal compartments.
There are 4 classifications of autophagy: 1) macroautophagy, 2) microautophagy, 3) crinophagy, and 4) chaperone-mediated autophagy (CMA). Among them, macroautophagy and microautophagy are highly conserved, involving distinctive membrane dynamics which are under the regulation of multiple autophagy-related proteins along with other molecules, and some of these modulators are shared by the two pathways.
There are numerous molecules partaking in the modulation of autophagy. Typical autophagy is a process with multiple phases that are mediated by the sequential and selective recruitment of the autophagy related (ATG) proteins, dominating a complex regulation network. The molecules involved in the pathways include: MTORC1, ATG13, ULK1, RB1CC1, ATG101, ATG9, AMPK, ULK1, BECN1, PIK3C3/VPS34, PIK3R4/VPS15, ATG14, NRBF2 BECN1‐PIK3C3/VPS34 complex, UVRAG, SH3GLB1, AMBRA1, RUBCN, BCL2, WIPI, ATG7, ATG10, ATG5, ATG12, ATG16L1, ATG3, ATG4, ATG 8‐family proteins (including mammalian MAP1LC3/LC3), Lipidated LC3, SQSTM1/p62, AKT1S1, DEPTOR, MLST8, RPTOR, etc.
Fig.1 Core regulation of canonical autophagy.1
Autophagy takes essential parts in intercellular communication, processes of non‐canonical secretion of proteins, functions of immune cells, tissue‐resident stem cell modulation, and maintenance of tissue barrier integrity. It also serves crucial roles in a wide range of human diseases, since dysregulation of autophagy is closely involved with the pathogenesis of cancers and other major human disorders including cardiovascular, metabolic, neurodegenerative, pulmonary, infectious, renal, ocular, and musculoskeletal disorders, as well as inflammations and aging. Taken together, autophagy and related genes or pathways have attracted increasing research interests for clinical research and drug development. Extensive efforts have been spurred to identify clinically available targets to exert regulation on the autophagic pathway to prevent, diagnose, or treat diseases.
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