| Theme | Parathyroid diseases and their pathogenesis | |
|---|---|---|
| Title | Role of FGF-23-Klotho in hyperparathyroidism | |
| Publish Date | 2013/11 | |
| Author | Kazuhiro Shiizaki | Department of Pathology, The University of Texas Southwestern Medical Center at Dallas |
| Author | Makoto Kuro-o | Department of Pathology, The University of Texas Southwestern Medical Center at Dallas |
| [ Summary ] | Klotho and FGF-23 play important roles in bone and mineral metabolism including endocrine regulation of phosphate and vitamin D metabolism. CKD-induced adaptation of this endocrine axis may contribute to secondary hyperparathyroidism. Klotho is essential for FGF-23 signaling as a co-receptor of FGF receptor. Decreased Klotho expression levels in the kidneys may increase circulating FGF-23 levels. FGF-23 suppresses the activation of vitamin D, resulting in secondary hyperparathyroidism. In the early stages of CKD, increased FGF-23 and PTH levels compensate for decreased functional nephron numbers to maintain the homeostasis of phosphate and calcium. Recent studies have revealed that PTH is also regulated by Klotho and FGF-23. It is proposed that resistance of the parathyroid glands to FGF-23 may contribute to secondary hyperparathyroidism. |
|