Does Fgf23-klotho activity influence vascular and soft tissue calcification through regulating mineral ion metabolism?

Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts, USA.
Kidney International (Impact Factor: 8.52). 07/2008; 74(5):566-70. DOI: 10.1038/ki.2008.218
Source: PubMed

ABSTRACT Recent studies describe a novel role of fibroblast growth factor-23 (Fgf23)-klotho activity in the systemic regulation of calcium and phosphate homeostasis. Both Fgf23 and klotho ablated mice develop extensive vascular and soft tissue calcification. Inability to clear the required amount of phosphate by the kidney, due to the absence of Fgf23-klotho activity, leads to increased accumulation of serum phosphate in these genetically modified mice, causing extensive calcification. Serum calcium and 1,25 hydroxyvitamin D levels are also elevated in both Fgf23 and klotho ablated mice. Moreover, increased sodium phosphate co-transporter activity in both Fgf23 and klotho ablated mice increases renal phosphate reabsorption which in turn can facilitate calcification. Collectively, these observations bring new insights into our understanding of the roles of the Fgf23-klotho axis in the development of vascular and soft tissue calcification.

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