期刊
AUTOPHAGY
卷 18, 期 10, 页码 2498-2499出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2022.2095788
关键词
Autophagy cargo receptors; extracellular vesicles; lysosome; proteostasis; secretory autophagy; vesicular trafficking
类别
资金
- NIH [CA201849, CA126792, CA213775, AG057462]
- Samuel Waxman Cancer Research Foundation
- Mark Foundation for Cancer Research
- UCSF QB3 Calico Longevity Fellowship
- Government of Canada [201409BPF-335868]
- Cancer Research Society Scholarship for Next Generation of Scientists [22805]
A novel secretory autophagy pathway called secretory autophagy during lysosome inhibition (SALI) was uncovered, which employs extracellular vesicles (EVs) and nanoparticles (EVPs) for the secretion of autophagy cargo receptors outside the cell when autophagosome maturation or lysosomal function is blocked.
Both macroautophagy/autophagy and extracellular vesicle (EV) secretion pathways converge upon the endolysosome system. Although lysosome impairment leads to defects in autophagic degradation, the impact of such dysfunction on EV secretion remains poorly understood. Recently, we uncovered a novel secretory autophagy pathway that employs EVs and nanoparticles (EVPs) for the secretion of autophagy cargo receptors outside the cell when either autophagosome maturation or lysosomal function is blocked. We term this process secretory autophagy during lysosome inhibition (SALI). SALI functionally requires multiple steps in classical autophagosome formation and the small GTPase RAB27A. Because the intracellular accumulation of autophagy cargo receptors perturbs cell signaling and quality control pathways, we propose that SALI functions as a failsafe mechanism to preserve protein and cellular homeostasis when autophagic or lysosomal degradation is impaired.
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