Fibroblast growth factor-23 remodels vascular extracellular matrix via glycosaminoglycan induction: implications for calcification in chronic kidney disease.

ABSTRACT: Chronic kidney disease (CKD) leads to accumulation of uremic toxins, which contribute to cardiovascular disease (CVD) and mortality. Among these, fibroblast growth factor 23 (FGF-23), a bone-derived hormone, is associated with arterial stiffness, vascular calcification, and left ventricular hypertrophy. However, the mechanisms linking elevated FGF-23 levels to vascular alterations remain poorly understood. We hypothesized that FGF-23 modulates the expression of sulfated glycosaminoglycans (sGAGs) and hyaluronic acid (HA) in vascular cells. Rat vascular smooth muscle cells (VSMCs) and human endothelial cells (ECs) were treated with FGF-23 ± its co-receptor Klotho and analyzed using qPCR, Western blotting, Blyscan assay, Alcian blue staining, ELISA, and reporter assays. FGF-23 significantly

SUBMITTER: Freise C 

PROVIDER: S-EPMC12507111 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature