Hannes Olauson

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.

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