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Autophagy in age-related macular degeneration using Vldlr KO mouse model of retinopathy

ABSTRACT: Autophagy in age-related macular degeneration using Vldlr KO mouse model of retinopathy

PROVIDER: PRJNA434120 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6726740_1.fastq.gz	Fastqsanger.gz
	SRR6726740_2.fastq.gz	Fastqsanger.gz
	SRR6726750_1.fastq.gz	Fastqsanger.gz
	SRR6726750_2.fastq.gz	Fastqsanger.gz
	SRR6726741_1.fastq.gz	Fastqsanger.gz

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Autophagy in age-related macular degeneration using Vldlr KO mouse model of retinopathy

Project description:Autophagy plays vital housekeeping neuronal functions but is not believed to fuel energy metabolism. Autophagy regulation by lipids nutrient sensors have not been identified. Cone photoreceptors’ very-low-density lipoprotein receptor (Vldlr) expression facilitates the uptake of triglyceride-derived fatty acid. In Vldlr-/- mice, we identify free fatty acid receptor 1 (Ffar1) as a suppressor of transcription factor EB (Tfeb), a master regulator of autophagy. Tfeb, in turn, governs the expression of PGC1 and Sirtuin-3, leading to reduced -ketoglutarate (-KG). We recently showed that low -KG in Vldlr-/- photoreceptors drives Vegfa expression and neovascularization reminiscent of a subset of age-related macular degeneration (AMD). Metabolomics of human AMD vitreous and Vldlr-/- retinas identified a similar Krebs cycle metabolite signature. Improving autophagy in AMD-like mice rescued the neovascular phenotype and vision. Dysregulated autophagy may therefore compound the energy failure of photoreceptors contributing to neovascular AMD and could be a driving force in other neovascular diseases.

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Impaired RPE Mitochondrial Energetics Leads Subretinal Fibrosis in Neovascular Age-related Macular Degeneration

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