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Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism.
Nat Rev Nephrol. 2013 Nov; 9(11):650-60.NR

Abstract

High concentrations of extracellular phosphate are toxic to cells. Impaired urinary phosphate excretion increases serum phosphate level and induces a premature-ageing phenotype. Urinary phosphate levels are increased by dietary phosphate overload and might induce tubular injury and interstitial fibrosis. Extracellular phosphate exerts its cytotoxic effects by forming insoluble nanoparticles with calcium and fetuin-A; these nanoparticles are referred to in this Review as calciprotein particles. Calciprotein particles are highly bioactive ligands that can induce various cellular responses, including the osteogenic transformation of vascular smooth muscle cells and cell death of vascular endothelial cells and renal tubular epithelial cells. Calciprotein particles are detected in the serum of animal models of kidney disease and in patients with chronic kidney disease (CKD) and might be associated with a (mal)adaptation of the endocrine axes mediated by fibroblast growth factors and Klothos that regulate phosphate homeostasis and ageing. These observations raise the possibility that calciprotein particles contribute to the pathogenesis of CKD. This theory, if verified, is expected to provide novel diagnostic markers and therapeutic targets in CKD.

Authors+Show Affiliations

Department of Pathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9072, USA. makoto.kuro-o@utsouthwestern.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

23774819

Citation

Kuro-o, Makoto. "Klotho, Phosphate and FGF-23 in Ageing and Disturbed Mineral Metabolism." Nature Reviews. Nephrology, vol. 9, no. 11, 2013, pp. 650-60.
Kuro-o M. Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism. Nat Rev Nephrol. 2013;9(11):650-60.
Kuro-o, M. (2013). Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism. Nature Reviews. Nephrology, 9(11), 650-60. https://doi.org/10.1038/nrneph.2013.111
Kuro-o M. Klotho, Phosphate and FGF-23 in Ageing and Disturbed Mineral Metabolism. Nat Rev Nephrol. 2013;9(11):650-60. PubMed PMID: 23774819.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Klotho, phosphate and FGF-23 in ageing and disturbed mineral metabolism. A1 - Kuro-o,Makoto, Y1 - 2013/06/18/ PY - 2013/6/19/entrez PY - 2013/6/19/pubmed PY - 2014/10/29/medline SP - 650 EP - 60 JF - Nature reviews. Nephrology JO - Nat Rev Nephrol VL - 9 IS - 11 N2 - High concentrations of extracellular phosphate are toxic to cells. Impaired urinary phosphate excretion increases serum phosphate level and induces a premature-ageing phenotype. Urinary phosphate levels are increased by dietary phosphate overload and might induce tubular injury and interstitial fibrosis. Extracellular phosphate exerts its cytotoxic effects by forming insoluble nanoparticles with calcium and fetuin-A; these nanoparticles are referred to in this Review as calciprotein particles. Calciprotein particles are highly bioactive ligands that can induce various cellular responses, including the osteogenic transformation of vascular smooth muscle cells and cell death of vascular endothelial cells and renal tubular epithelial cells. Calciprotein particles are detected in the serum of animal models of kidney disease and in patients with chronic kidney disease (CKD) and might be associated with a (mal)adaptation of the endocrine axes mediated by fibroblast growth factors and Klothos that regulate phosphate homeostasis and ageing. These observations raise the possibility that calciprotein particles contribute to the pathogenesis of CKD. This theory, if verified, is expected to provide novel diagnostic markers and therapeutic targets in CKD. SN - 1759-507X UR - https://www.unboundmedicine.com/medline/citation/23774819/Klotho_phosphate_and_FGF_23_in_ageing_and_disturbed_mineral_metabolism_ L2 - https://doi.org/10.1038/nrneph.2013.111 DB - PRIME DP - Unbound Medicine ER -