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PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy [MG_HG]

GSE304690 Homo sapiens Expression profiling by high throughput sequencing 10 samples 2025/08/11 GPL34284
Summary
In diabetic retinopathy (DR), hyperglycemia induces retinal pigment epithelium (RPE) cell senescence via downregulation of PDZK1. PDZK1 overexpression counteracts senescence by binding 14-3-3ε to modulate mTOR signaling, reducing oxidative stress and enhancing autophagy. Both genetic PDZK1 restoration and pharmacologic senolysis (Nutlin-3a) attenuate retinal senescence and ameliorate early DR pathology, establishing the PDZK1-14-3-3ε-mTOR axis as a therapeutic target
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NCBI GEO page ↗ Paper (PMID 40853330) ↗ {# Names what the click gives you. "Open in finder" meant nothing to a visitor who arrived from a search engine and has never seen the tool. #} Find more human RNA-seq datasets →
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