Fgf23

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Federal government websites often end in. The site is secure. Abnormalities of FGF23 production underlie many inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts. The parathyroid hormone PTH -vitamin D axis has provided the basis for our conceptualization of bone and mineral homeostasis, but recent discovery of the fibroblast growth factor FGF 23 bone-kidney axis regulating vitamin D metabolism and renal phosphate handling have led to new insights into physiology and pathophysiology of mineral metabolism. Comprehensive reviews of vitamin D metabolism and PTH functions have been published previously in this journal

Fgf23

Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. The bone-derived hormone fibroblast growth factor 23 FGF23 functions in concert with parathyroid hormone PTH and the active vitamin D metabolite, 1,25 OH 2 vitamin D 1,25D , to control phosphate and calcium homeostasis. A rise in circulating levels of phosphate and 1,25D leads to FGF23 production in bone. Various other biomolecules that are produced by the kidney, including lipocalin-2, glycerol 3-phosphate, 1-acyl lysophosphatidic acid and erythropoietin, are involved in the regulation of mineral metabolism via effects on FGF23 synthesis in bone. Understanding of the molecular mechanisms that control FGF23 synthesis in the bone and its bioactivity in the kidney has led to the identification of potential targets for novel interventions. The osteocyte-derived hormone fibroblast growth factor 23 FGF23 controls renal handling of phosphate and active 1,25 OH 2 vitamin D 1,25D. Rare heritable and common acquired disturbances in FGF23 homeostasis, including chronic kidney disease, are associated with altered mineral balance. The regulation of FGF23 production in osteocytes occurs via transcriptional and post-translational mechanisms. Identification of the mechanisms of FGF23 functions and the effects of FGF23 on downstream targets in the kidney could lead to the development of novel therapeutics. This is a preview of subscription content, access via your institution.

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Fibroblast growth factor 23 FGF23 is a protein and member of the fibroblast growth factor FGF family which participates in the regulation of phosphate in plasma and vitamin D metabolism. In humans it is encoded by the FGF23 gene. FGF23 decreases reabsorption of phosphate in the kidney. Mutations in FGF23 can lead to its increased activity, resulting in autosomal dominant hypophosphatemic rickets. It does this by decreasing reabsorption of phosphate in the kidney, which means phosphate is excreted in urine. FGF23 is secreted by osteocytes in response to increased calcitriol and phosphate. FGF23 may also suppress 1-alpha-hydroxylase , reducing its ability to activate vitamin D and subsequently impairing calcium absorption.

Federal government websites often end in. The site is secure. The data supporting this review are from previously reported studies and datasets, which have been cited at relevant places within the text as references [ 1 — ]. FGF23 is a hormone secreted mainly by osteocytes and osteoblasts in bone. Its pivotal role concerns the maintenance of mineral ion homeostasis.

Fgf23

Federal government websites often end in. The site is secure. Cyril and Methodius, Skopje, North Macedonia. Fibroblast growth factor 23 FGF23 is a phosphaturic hormone produced mainly in osteocytes. In chronic kidney disease CKD FGF23 levels increase due to higher production, but also as the result of impaired cleavage and reduced excretion from the body. FGF23 has a significant role in disturbed bone and mineral metabolism in CKD, which leads to a higher cardiovascular risk and mortality in these patients. Current research has emphasized the expression of FGF23 in cardiac myocytes, fibroblasts, and endothelial cells, and in addition to the effects on the kidney, its primary role is in cardiac remodeling in CKD patients. Under normal physiological conditions, the kidney maintains soluble Klotho homeostasis, whereas chronic kidney disease CKD patients had lower klotho mRNA expression in the kidney following the decline of kidney function [ 5 ]. FGF23 is secreted primarily by osteocytes to maintain phosphate and mineral homeostasis. Its physiological effect on renal functions is mediated through binding to FGF receptor FGFR 1 in the proximal tubular cells in the presence of its co-factor klotho.

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Klotho: a novel phosphaturic substance acting as an autocrine enzyme in the renal proximal tubule. J Orthop Res. Mol Cell Endocrinol — Independent impairment of osteoblast and osteoclast differentiation in klotho mouse exhibiting low-turnover osteopenia. Molecular and Structural Endocrinology. J Bone Miner Res —7. Wang Y, Sun Z. Fibroblast growth factor 23 signals the kidneys to stop reabsorbing phosphate into the bloodstream. Klotho protein activates the PKC pathway in the kidney and testis and suppresses hydroxyvitamin D 3 1alpha-hydroxylase gene expression. This is a preview of subscription content, access via your institution. There is an association of increased FGF23 and plasma cell dyscrasias , but a formal assessment of the effect of increased osteoclastic mediated bone resorption of FGF23 expression in bone has not been performed. Fgf23 deficient mice are characterized by increased erythropoiesis Portale, A. To be secreted from the cell, sugar molecules are attached to fibroblast growth factor 23 by another protein called ppGalNacT3 in a process called glycosylation.

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Molecular insights into the Klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members. Biochem J. The regulation of FGF23 production in osteocytes occurs via transcriptional and post-translational mechanisms. Haematologica , e—e Selective pharmacological inhibition of the sodium-dependent phosphate cotransporter NPT2a promotes phosphate excretion. J Clin Invest — Nephrol Dial Transplant. Conditional deletion of MurineFgf interruption of the normal skeletal responses to phosphate challenge and rescue of genetic hypophosphatemia. Consistently, estrogens correlated in a dose-dependent manner with the magnitude of the FGF23 increments, suggesting that estrogens may be a potent stimulator for FGF23 Dupont J, Holzenberger M. Both the phosphaturic and the 1,25 OH 2 D 3 -lowering effect of FGF23 protect against hyperphosphatemia: the first effect directly through increased elimination of phosphate, and the second effect indirectly through reduced intestinal phosphate absorption. Nature —4.