GEO series

HNF1B integrates signals in a feed-forward loop driving kidney disease progression [RNAseq_UUOd1]

GSE297989 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2026/04/21 Platform GPL24247

Summary

Chronic kidney disease (CKD) is a complex disorder with substantial unexplained heritability. While GWAS have identified common variants, rare variants and gene-environment interactions likely play a major role. HNF1B, a transcription factor essential for kidney development, is also a cause of monogenic CKD but its function in adult kidneys remains unclear. Here, we show that HNF1B loss in adult mouse kidneys induces rapid CKD with epithelial dedifferentiation, aberrant cell cycle re-entry, and replicative stress. Strikingly, suppression of the HNF1B transcriptional program is observed across multiple human and experimental CKD models, independent of cause. These findings position HNF1B as a central regulator of renal epithelial integrity and reveal a feed-forward mechanism in which HNF1B dysfunction contributes to and is reinforced by CKD progression. Our results provide insight into shared pathways underlying diverse forms of CKD and suggest new targets for therapeutic intervention.

Published in

HNF1B integrates signals in a feed-forward loop driving kidney disease progression

Isnard P, Makinistoglu MP, Leibovici M et al. · Science (New York, N.Y.) 2026 · PMID 41990178 · doi:10.1126/science.aea3219

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Direct links to NCBI, no account and no request form: the whole study as GSE297989_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Whole study · RAW.tar ↓ Series matrix ↓ All supplementary files ↗ Raw reads on ENA ↗

Also filed as BioProject PRJNA1267081 and SRA study SRP587385. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41990178) ↗

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