Nephrotic syndrome in mice elevates FGF23 levels and leads to cardiac hypertrophy in the absence of hyperphosphatemia
Our study suggests that NFATc1nuc mice serve as a model of nephrotic syndrome that progresses to CKD with pathologic cardiac remodeling. Our findings indicate that hyperlipidemia might contribute to heart failure in nephrotic syndrome by inducing FGF23 expression in the heart, which then drives cardiac hypertrophy.
Authors
- Kylie Heitman (ORCID: https://orcid.org/0000-0002-5345-2727)
- Alexis Sloan
- Alessia Fornoni (ORCID: https://orcid.org/0000-0002-1313-7773)
- Abul Fajol (ORCID: https://orcid.org/0000-0002-3202-5697)
- Christopher Yanucil
- Orlando M. Gutiérrez (ORCID: https://orcid.org/0000-0001-6593-3571)
- Min Xie (ORCID: https://orcid.org/0009-0002-2828-8096)
- Dominik Kentrup (ORCID: https://orcid.org/0000-0003-3887-4304)
- Alexander Grabner (ORCID: https://orcid.org/0000-0002-5544-1896)
- Christian Faul (ORCID: https://orcid.org/0000-0002-7512-0977)
- Qing Li (ORCID: https://orcid.org/0000-0001-8218-7929)
- Lihao He (ORCID: https://orcid.org/0000-0001-8361-032X)
- Sandra Merscher
- S Madison Thomas
Institutions
- University of Miami (US)
- Universität Hamburg (DE)
- University of Alabama at Birmingham (US)
- University Medical Center Hamburg-Eppendorf (DE)
Publication Details
- Journal
- Nephrology Dialysis Transplantation
- Published
- 2025-12-22
- DOI
- https://doi.org/10.1093/ndt/gfaf272
- Citations
- 1
- Primary Topic
- Parathyroid Disorders and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 1.43