{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gegnaw ST"],"funding":["Centre National de la Recherche Scientifique (CNRS)","EC | Chafea | Consumer Programme (Consumer Programme - European Commission)","Consumer Programme","Centre National de la Recherche Scientifique"],"pagination":["e70507"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11962828"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(7)"],"pubmed_abstract":["Daily rhythms are a central hallmark of vision, in particular by adapting retinal physiology and light response to the day-night cycle. These cyclic processes are regulated by retinal circadian clocks, molecular machineries regulating gene expression across the 24-h cycle. Although hundreds of genes associated with genetic retinal disorders have been identified, no direct link has been established with the clock. Hence, we investigated the hypothesis that a poorly functioning circadian clock aggravates retinal photoreceptor disease. We performed this study in the P23H rhodopsin-mutated mouse model (P23H Rho) that mimics one major cause of human autosomal dominant retinitis pigmentosa. We also used the rod-specific knockout (rod-Bmal1KO) of Bmal1, a key clock component. More specifically, w"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Circadian clock disruption promotes retinal photoreceptor degeneration."],"pmcid":["PMC11962828"],"funding_grant_id":["NeuroTime Erasmus+ grant","Core funding"],"pubmed_authors":["Moerland PD","Felder-Schmittbuhl MP","Gegnaw ST","Ten Brink JB","Milicevic N","Jongejan A","Bergen AA","Sandu C","Bery A"],"additional_accession":[]},"is_claimable":false,"name":"Circadian clock disruption promotes retinal photoreceptor degeneration.","description":"Daily rhythms are a central hallmark of vision, in particular by adapting retinal physiology and light response to the day-night cycle. These cyclic processes are regulated by retinal circadian clocks, molecular machineries regulating gene expression across the 24-h cycle. Although hundreds of genes associated with genetic retinal disorders have been identified, no direct link has been established with the clock. Hence, we investigated the hypothesis that a poorly functioning circadian clock aggravates retinal photoreceptor disease. We performed this study in the P23H rhodopsin-mutated mouse model (P23H Rho) that mimics one major cause of human autosomal dominant retinitis pigmentosa. We also used the rod-specific knockout (rod-Bmal1KO) of Bmal1, a key clock component. More specifically, w","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-07-15T11:10:29.017Z","creation":"2025-07-11T03:03:53.224Z"},"accession":"S-EPMC11962828","cross_references":{"pubmed":["40171795"],"doi":["10.1096/fj.202401967R"]}}