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Crosstalk between Endo/Exocytosis and Autophagy in Health and Disease
Imbalance between the main intracellular degradative, trafficking and intercellular shuttling pathways has been implicated in disease pathogenesis. Autophagy controls degradation of cellular components, while vesicular trafficking permits transport of material in and out of the cell. Emerging eviden...
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Published in: | Biotechnology journal 2020-08, Vol.15 (8), p.e1900267-n/a |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Imbalance between the main intracellular degradative, trafficking and intercellular shuttling pathways has been implicated in disease pathogenesis. Autophagy controls degradation of cellular components, while vesicular trafficking permits transport of material in and out of the cell. Emerging evidence has uncovered the extensive interconnectivity between these pathways, which is crucial to maintain organismal homeostasis. Thus, therapeutic intervention and drug development strategies targeting these processes, particularly in neurodegeneration, should account for this broad crosstalk, to maximize effectiveness. Here, recent findings underlining the highly dynamic nature of the crosstalk between autophagy, endosomal transport, and secretion is reviewed. Synergy of autophagy and endosomes for degradation, as well as, competition of autophagy and secretion are discussed. Perturbation of this crosstalk triggers pathology especially neurodegeneration.
The crosstalk between endocytosis and exocytosis, and autophagy is extensive and multifaceted. Endosomes, contribute to the activation of autophagy, the formation and maturation of autophagosomes, and their fusion with lysosomes. Conversely, when digestive autophagy is repressed, autophagic secretion of intracellular components, including signaling molecules, contained in exosomes, ensues. Imbalance of this crosstalk has been implicated in neurodegeneration and autoimmune disorders. |
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ISSN: | 1860-6768 1860-7314 |
DOI: | 10.1002/biot.201900267 |