| Theme | Chronic kidney disease and aging -- Phosphate connection | |
|---|---|---|
| Title | Renal senescence | |
| Publish Date | 2015/01 | |
| Author | Naoki Kashihara | Department of Nephrology and Hypertension, Kawasaki Medical School |
| Author | Minoru Satoh | Department of Nephrology and Hypertension, Kawasaki Medical School |
| [ Summary ] | The klotho mutant mice exhibit premature aging syndrome, which is also observed in patients with end stage renal disease. A deficiency of the intrinsic factor produced in kidneys, Klotho protein, may result in the aging phenotype (renal senescence hypothesis). Klotho converts canonical FGF receptor into a specific receptor for FGF23 and plays an essential role in phosphate metabolism. Impaired urinary phosphate excretion increases serum phosphate and fetuin-A-containing calciprotein particle levels and induces a premature-ageing phenotype. The soluble Klotho products serve as circulating factors and are implicated in renal fibrosis through regulation of multiple signaling pathways, including TGF-beta and Wnt/beta-catenin. Kidney injury is assumed to be involved in the development of premature aging syndrome. The preservation of kidney function may lead to prolongation of healthy life spans. |
|