Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5705670 | Progress in Retinal and Eye Research | 2016 | 40 Pages |
Abstract
Autophagy is a catabolic pathway that promotes the degradation and recycling of cellular components. Proteins, lipids, and even whole organelles are engulfed in autophagosomes and delivered to the lysosome for elimination. In response to stress, autophagy mediates the degradation of cell components, which are recycled to generate the nutrients and building blocks required to sustain cellular homeostasis. Moreover, it plays an important role in cellular quality control, particularly in neurons, in which the total burden of altered proteins and damaged organelles cannot be reduced by redistribution to daughter cells through cell division. Research has only begun to examine the role of autophagy in the visual system. The retina, a light-sensitive tissue, detects and transmits electrical impulses through the optic nerve to the visual cortex in the brain. Both the retina and the eye are exposed to a variety of environmental insults and stressors, including genetic mutations and age-associated alterations that impair their function. Here, we review the main studies that have sought to explain autophagy's importance in visual function. We describe the role of autophagy in retinal development and cell differentiation, and discuss the implications of autophagy dysregulation both in physiological aging and in important diseases such as age-associated macular degeneration and glaucoma. We also address the putative role of autophagy in promoting photoreceptor survival and discuss how selective autophagy could provide alternative means of protecting retinal cells. The findings reviewed here underscore the important role of autophagy in maintaining proper retinal function and highlight novel therapeutic approaches for blindness and other diseases of the eye.
Keywords
LPSHMALSDCMAERGEGCGHsc70RGCAMDMCTAGEshsp70ASMLMPMPTGCLAAVMNUiOpRPEUPRIPLINLONL5-(N,N-Hexamethylene)amilorideBRB3-MALAPRetinitis pigmentosaNTGONHTXNIPchaperone mediated autophagyN-methyl-N-nitrosoureaTGFBIpPI3Pgranular corneal dystrophy type 2ADOAPhotoreceptor outer segmentAdeno-associated vectorUbiquitin binding domainUbDLC3-associated phagocytosis8-OH DPATTAK-1lysosomal cell deathTLK3-methyl adenine8-hydroxy-2-(di-n-propylamino)-tetralinChaperone-mediated autophagyBDNFLysosomal membrane permeabilizationROSautosomal dominant optic atrophyAutophagyLysosomal storage disorderLCDelectroretinogramOptic nerve transectionmitochondrial permeability transitionretinal pigment epitheliumepigallocatechin gallateLIRBis(monoacylglycero)phosphateCNSMacular degenerationRetinal dystrophiesdiabetic retinopathyembryonic dayOptic nerve headRetinal pigment epithelial cellsRetinal ganglion cellsretinal ganglion cellage-related macular degenerationSipscentral nervous systemendoplasmic reticulumtrabecular meshworkRetinaVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)Brain-derived neurotrophic factorPhotoreceptorphosphatidylinositol 3-phosphateIntraocular pressureTRAILouter nuclear layerinner plexiform layerinner nuclear layerganglion cell layerLysosomeslow density lipoproteinLDLlipopolysaccharidetumour necrosis factor-related apoptosis-inducing ligandBMPProtease inhibitorsMitophagyUnfolded protein responsethioredoxin-interacting proteinheat shock protein 70Rho-associated protein kinaseposStress-induced premature senescenceGlaucomanormal tension glaucomaReactive oxygen speciesRock
Related Topics
Life Sciences
Neuroscience
Sensory Systems
Authors
Patricia Boya, Lorena Esteban-MartÃnez, Ana Serrano-Puebla, Raquel Gómez-Sintes, Beatriz Villarejo-Zori,