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Methyglyoxal reshapes the transcriptional network of human retinal endothelial cells [RNA-seq]

GSE263471 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/06/30 Platform GPL24676
Summary
Diabetic retinopathy (DR) is a complex microvascular complication of diabetes and a leading cause of vision impairment. A primary event of DR is the functional impairment of microvascular cells (i.e., pericytes and endothelial cells) and pathological changes in the retinal neurovascular unit. In diabetes-related complications, advanced glycation end products (AGEs) play a pivotal role in oxidative damage induced by chronic hyperglycemia particularly in damaging retinal endothelial cells. Methylglyoxal (MGO) is the most reactive AGE precursor, able to induce vascular damage, neuroretinal dysfunction and retinal lesions. Here, we demonstrate that sublethal doses of MGO induce protein glycation adduct formation in human retinal endothelial cells (hRECs), impairing the migratory and tube-forming capabilities. Moreover, transcriptome and miRNome analyses highlighted extensive perturbations in gene expression and microRNA profiles, especially related to gene expression regulation, cell cycle, cell death and vasculature development.
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Direct links to NCBI, no account and no request form: the whole study as GSE263471_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1097600 and SRA study SRP500397. Searching any of these in the dataset finder brings you back here.

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