Matthias B. Moor

The paper identifies a STAT1-CEBPB-NF-κB signaling pathway in diabetic kidneys that mediates FGF23's pro-inflammatory effects, suggesting CEBPB as a therapeutic target.

This study shows high-salt diets increase urinary cortisol and decrease plasma FGF23, revealing a novel endocrine interaction with implications for bone, kidney, and cardiovascular health.

The paper uses precision-cut kidney slices from BXD mouse strains to model nephrotoxicity ex vivo, finding strain-specific differences in susceptibility to drug-induced kidney injury.

This study shows that excess FGF23 drives inflammation in kidney disease models and human data, suggesting it as a therapeutic target.

The paper uses single-cell RNAseq data to analyze genetic factors influencing cell-type composition in mouse tissues, identifying heritability and QTLs associated with cell-type abundance.

This study shows that overexpressing Fgf23 in male ApoE-/- mice increases atherosclerotic plaque burden and alters immune responses.

This study shows that chronic FGF23 elevation causes kidney inflammation via sustained ERK signaling, which is reduced by cFGF23 gene therapy.

This study compares precision-cut kidney slices (PCKS) with pig kidney transplantation to model ischemia-reperfusion injury, finding that PCKS recapitulates post-reperfusion gene expression patterns seen in human kidney transplantation.