Matthias B. Moor

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.