Abstract
Mice lacking Klotho or fibroblast growth factor 23 (FGF23) exhibit a premature aging syndrome associated with abnormal mineral metabolism characterized by hyperphosphatemia, hypercalcemia, and hypervitaminosis D. Several genetic and dietary interventions that reduce blood phosphate, calcium, and/or vitamin D levels rescue the premature aging syndrome concomitantly. Notably, the rescue is always associated with decrease in blood phosphate levels, but not necessarily with decrease in calcium or vitamin D, suggesting that hyperphosphatemia is primarily responsible for the premature aging. Hyperphsophatemia, decreased Klotho expression, and aging-like symptoms are often manifested in patients with chronic kidney disease (CKD). Thus, CKD may be viewed as a premature aging syndrome caused by hyperphosphatemia and Klotho deficiency. Further clinical studies are required to verify the link between phosphate and aging and to apply this novel concept to anti-aging medicine.
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