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

GSE304545 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/08/12 Platform 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
Published in
PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy
Zhao J, Zhang J, Liu Y et al. · Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2025 · PMID 40853330 · doi:10.1002/advs.202511288
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Also filed as BioProject PRJNA1301643 and SRA study SRP606706. Searching any of these in the dataset finder brings you back here.

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