The renal response to FGF23 shifts from phosphaturia towards inflammation in kidney disease
Matthias B. Moor, Mikhail Burmakin, Anna Levin, Gül Gizem Korkut, David Brodin, Annika M. Wernerson, Annette N. Bruchfeld, Peter F. Barany, Anna Witasp, Jaakko Patrakka, Hannes Olauson
This study shows that excess FGF23 drives inflammation in kidney disease models and human data, suggesting it as a therapeutic target.
Journal of Cell Communication and Signaling · Feb 23, 2026Peer-reviewedMolecular Biology