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Transcriptomic analysis of kidney cortex following knockdown of endothelial Klf4 on wild-type and Nos3 deficient backgrounds.

GSE274856 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/07/23 Platform GPL24247
Summary
The goal of this study was to identify transcriptomic changes, mediated by the loss of endothleial Klf4, seen in glomerular microangiopathy in kidney endothelial cells. We recently reported that the endothelial-specific knockout of Krüppel-like factor 4 (Klf4) increases the susceptibility to GEnC injury and subsequent development of subacute thrombotic microangiopathy. However, the mechanism(s) mediating GEnC response to injury in thrombotic microangiopathy are poorly understood. Single nucleus RNA sequencing demonstrated an enrichment in pathways involved in angiogenesis, permeability, focal adhesion and cytoskeletal organization, specifically in the endothelial cluster in mice with endothelial loss of Klf4.
Published in
Induction of plasmalemmal vesicle-associated protein exacerbates glomerular endothelial injury in thrombotic microangiopathy
Estrada CC, Wilson C, Gujarati N et al. · American journal of physiology. Renal physiology 2025 · PMID 39706169 · doi:10.1152/ajprenal.00283.2024
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Also filed as BioProject PRJNA1148198 and SRA study SRP526423. Searching any of these in the dataset finder brings you back here.

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