Fibroblast growth factor 23 and uremic vascular calcification: is it time to escalate from biomarker status to pathogenic agent?
Although epidemiologic associations have been informative, the elucidation of the role of fibroblast growth factor 23 (FGF23) in chronic kidney disease (CKD) requires testing with robust experimental models. Jimbo et al. used animal and cell-culture models to query whether FGF23 is a direct 'vasculotoxin.' We discuss the interpretation of their findings. At this juncture, much remains unanswered about the significance of FGF23 elevation in CKD.
1] Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA [2] Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA [3] Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Orson W
OW
Moe
1] Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA [2] Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Makoto
M
Kuro-o
D000818:Animals; D001018:Aortic Diseases / Q000139:chemically induced*; D005346:Fibroblast Growth Factors / Q000633:toxicity*; D005966:Glucuronidase / Q000378:metabolism*; D000090265:Klotho Proteins; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D010710:Phosphates / Q000633:toxicity*; D061205:Vascular Calcification / Q000139:chemically induced*
C505605:Fgf23 protein, rat; D010710:Phosphates; D005346:Fibroblast Growth Factors; D005966:Glucuronidase; D000090265:Klotho Proteins; C018279:sodium phosphate