| Theme | Chronic kidney disease and aging -- Phosphate connection | |
|---|---|---|
| Title | Physiology of FGF23-Klotho endocrine system | |
| Publish Date | 2015/01 | |
| Author | Kazuhiro Shiizaki | Department of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University |
| Author | Yutaka Miura | Department of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University |
| Author | Hiroshi Kurosu | Department of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University |
| Author | Makoto Kuro-o | Department of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University |
| [ Summary ] | Klotho has been identified as an anti-aging gene which extends life spans when over-expressed and induces a premature aging syndrome when disrupted in mice. Klotho is expressed primarily in the kidneys and parathyroid glands, where it forms binary complexes with fibroblast growth factor receptors (FGFRs) to serve as an obligatory co-receptor of fibroblast growth factor-23 (FGF23). FGF23 is a hormone which promotes phosphate excretion into the urine and reduces the active form of vitamin D in the serum. Thereby, it plays critical roles in the endocrine regulation of phosphate and vitamin D homeostasis. Adaptation and malfunction of the FGF23-Klotho endocrine axis is universally observed in chronic kidney disease (CKD), which is associated with various aging-like phenotypes. We thus propose that CKD may be viewed as a premature aging syndrome caused by disorders of the FGF23-Klotho endocrine axis. | |