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• W2289711537 abstract "// Marina Zieger 1 and Claudio Punzo 1 1 Department of Ophthalmology and Gene Therapy Center, University of Massachusetts Medical School, Worcester MA, USA Correspondence to: Claudio Punzo, email: // Keywords : AMD, cone degeneration, rod degeneration, geographic atrophy, mTORC1, Gerotarget Received : September 18, 2015 Accepted : January 23, 2016 Published : February 11, 2016 Abstract Age-related macular degeneration (AMD) is characterized by malfunction and loss of retinal-pigmented epithelium (RPE) cells. Because the RPE transfers nutrients from the choriocapillaris to photoreceptor (PR), PRs are affected as well. Geographic atrophy (GA) is an advanced form of AMD characterized by severe vision impairment due to RPE loss over large areas. Currently there is no treatment to delay the degeneration of nutrient deprived PRs once RPE cells die. Here we show that cell-autonomous activation of the key regulator of cell metabolism, the kinase mammalian target of rapamycin complex 1 (mTORC1), delays PR death in the sodium iodate induced model of RPE atrophy. Consistent with this finding loss of mTORC1 in cones accelerates cone death as cones fail to balance demand with supply. Interestingly, promoting rod survival does not promote cone survival in this model of RPE atrophy as both, rods and cones suffer from a sick and dying RPE. The findings suggest that activation of metabolic genes downstream of mTORC1 can serve as a strategy to prolong PR survival when RPE cells malfunction or die." @default.
• W2289711537 created "2016-06-24" @default.
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• W2289711537 date "2016-02-11" @default.
• W2289711537 modified "2023-10-16" @default.
• W2289711537 title "Improved cell metabolism prolongs photoreceptor survival upon retinal-pigmented epithelium loss in the sodium iodate induced model of geographic atrophy" @default.
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• W2289711537 doi "https://doi.org/10.18632/oncotarget.7330" @default.
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