Mikhail Burmakin

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.

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 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.