Fgf23

Federal government websites often end in. The site is secure. Abnormalities of FGF23 production underlie fgf23 inherited and acquired disorders of phosphate homeostasis. This review discusses the known and emerging functions of FGF23, fgf23, its regulation in response to systemic and local signals, as well as the implications of FGF23 in different pathological and physiological contexts, 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.

Fgf23

Federal government websites often end in. The site is secure. Fibroblast growth factor FGF23 is a bone-derived hormone suppressing phosphate reabsorption and vitamin D hormone synthesis in the kidney. It is well established that excessive concentrations of intact FGF23 in the blood lead to phosphate wasting in patients with normal kidney function. Based on the importance of diseases associated with gain of FGF23 function such as phosphate-wasting diseases and chronic kidney disease, a large body of literature has focused on the pathophysiological consequences of FGF23 excess. Less emphasis has been put on the role of FGF23 in normal physiology. Moreover, FGF23 may be a physiological suppressor of differentiation of hematopoietic stem cells into the erythroid lineage in the bone microenvironment. At present, there is little evidence for a physiological role of FGF23 in organs other than kidney and bone. The purpose of this mini-review is to highlight the current knowledge about the complex physiological functions of FGF In the year , gain-of-function mutations in fibroblast growth factor FGF23 were identified as the genetic cause of autosomal dominant hypophosphatemic rickets ADHR , an inherited renal phosphate-wasting disease 1. The principal action of FGF23 on mineral metabolism that led to its discovery as a hormone is the suppressive effect on phosphate reabsorption from the urine 10 , It is now well known that diseases characterized by excessive blood concentrations of intact FGF23 lead to renal phosphate wasting and inappropriately low-circulating 1,25 OH 2 D 3 levels in patients with a normal kidney function In terms of factors that may drive FGF23 secretion, the common denominator in both diseases is impaired bone mineralization.

Although the defective skeletal mineralization observed in patients and animal models with FGF23 excess is likely a consequence of low phosphorus and vitamin D values, fgf23, FGF23 treatment of primary calvarial osteoblasts from wild-type mice and osteoblast-like cells leads to an inhibition of mineralization, fgf23. Homozygous ablation of fibroblast growth fgf23 results in hyperphosphatemia and impaired skeletogenesis, reverses hypophosphatemia in Phex-deficient mice.

Official websites use. Share sensitive information only on official, secure websites. The FGF23 gene provides instructions for making a protein called fibroblast growth factor 23, which is produced in bone cells. This protein is necessary in regulating the phosphate levels within the body phosphate homeostasis. Among its many functions, phosphate plays a critical role in the formation and growth of bones in childhood and helps maintain bone strength in adults.

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.

Fgf23

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.

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Fibroblast growth factor 23 regulates renal 1,dihydroxyvitamin D and phosphate metabolism via the MAP kinase signaling pathway in Hyp mice. Orthologs Species Human. Hence, although high-FGF23 blood concentrations may suppress PTH secretion in a Klotho-independent fashion in rodents 65 , 66 , it is unlikely that FGF23 signaling has an important role in the physiological regulation of PTH secretion. 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. This finding strongly suggests that the FGF23 and PTH-mediated regulation of hydroxylase expression are entirely indirect through altered 1,25 OH 2 D 3 synthesis and subsequent changes in VDR-regulated promoter activity of hydroxylase. Decreased expression of klotho gene in uremic atherosclerosis in apolipoprotein E-deficient mice. Sci Rep 7 These findings suggest that primary physiochemical-mediated impairment of mineralization can somehow stimulate FGF23 expression in bone. PLoS One 7:e American Journal of Physiology. E1 cell proliferation and inhibit mineralization. Mol Cell Biol 32 — Sorry, a shareable link is not currently available for this article. FGF23 neutralization improves chronic kidney disease-associated hyperparathyroidism yet increases mortality.

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This finding strongly suggests that the FGF23 and PTH-mediated regulation of hydroxylase expression are entirely indirect through altered 1,25 OH 2 D 3 synthesis and subsequent changes in VDR-regulated promoter activity of hydroxylase. The main functions of FGF23 are its systemic effects to 1 act as a counterregulatory hormone for 1,25 OH 2 D and 2 coordinate renal phosphate handling to match bone mineralization 40 , , , Additional data suggest that accumulation of ASARM as a consequence of inactivation of Phex can impair mineralization and phosphate homeostasis Nature , — The discovery that osteoblasts and osteocytes are the principal site for FGF23 production and secretion identified bone, not only as the major reservoir for calcium and phosphate, but as an endocrine organ that communicates with other organs involved in mineral homeostasis. Ther Apher Dial. Ethics declarations Competing interests K. Functions and regulations of fibroblast growth factor signaling during embryonic development. Inactivating mutations of Enpp1, which more typically causes hereditary generalized arterial calcification of infancy GACI , can also cause a variant of autosomal recessive hypophosphatemic rickets, characterized by hypophosphatemia and elevated FGF23 levels in some patients , Calcinosis results when the excess phosphate combines with calcium to form deposits that build up in soft tissues. No conflicts of interest, financial or otherwise, are declared by the authors. Sign up for Nature Briefing.