The abstract is read at the publisher; the summary is JClub's.
In streptozotocin-induced diabetic kidney disease in DBA/2J mice, FGF23 induces a disease-specific STAT1–CEBPB–NF-{kappa}B inflammatory transcriptional axis, with CEBPB inhibition suppressing pro-inflammatory programs.
- Why it matters: Elevated circulating FGF23 is linked to renal inflammation in diabetic kidney disease, but the specific renal cell programs and pathways mediating these off-target effects were unclear.
- What they did: DBA/2J mice received streptozotocin or vehicle, then received a single intravenous FGF23 dose (0.3 g) or vehicle; 1 h later, single-nucleus RNA sequencing and regulon analysis identified FGF23-driven transcription factor activity, tested in precision-cut kidney slices with the CEBPB inhibitor ST-101.
- The result: FGF23 responses were conserved for canonical targets yet added DKD-restricted induction of CEBPB regulon activity (and STAT1 in several segments), and ST-101 pre-treatment suppressed CEBPB activity, downstream NF-KB and pro-inflammatory gene sets, and immune-like cell abundance in diseased slices.
The findingWhy it mattersWhat they didThe result
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