Autophagy is a highly conserved housekeeping pathway that plays a critical role in the removal of aged or damaged intracellular organelles and their delivery to lysosomes for degradation. 1,2 Autophagy begins with the formation of membranes, arising in part from the endoplasmic reticulum, that elongate and fuse engulfing cytoplasmic constituents into a classic double-membrane bound nascent autophagosome. These early autophagosomes undergo a stepwise maturation process to form the late autophagosome or amphisome that ultimately fuses with a lysosome. Efficient autophagy is dependent on an equilibrium between the formation and elimination of autophagosomes; thus, a deficit in any part of this pathway will cause autophagic dysfunction. Autophagy plays a role in aging and agerelated diseases.1,2,7 However, few studies of autophagy in retinal disease have been reported. © 2009 Landes Bioscience.
CITATION STYLE
Wang, A. L., Boulton, M. E., Dunn, W. A., Rao, H. V., Cai, J., Lukas, T. J., & Neufeld, A. H. (2009). Using LC3 to monitor autophagy flux in the retinal pigment epithelium. Autophagy, 5(8), 1190–1193. https://doi.org/10.4161/auto.5.8.10087
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