Fgf23

Official websites use. Share sensitive information only on official, secure websites. The FGF23 gene provides instructions for making a protein called fibroblast fgf23 factor 23, which fgf23 produced in bone cells. This protein is necessary in regulating the phosphate levels within the body phosphate homeostasis, fgf23.

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.

Phosphate regulating gene with homologies to endopeptidases on the X chromosome PHEX is a kDa protein member of the endothelin-converting enzyme family expressed by osteoblasts and osteocytes fgf23 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.

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. Phosphate levels are controlled in large part by the kidneys.

Fgf23

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. It has been confirmed that phosphate and vitamin D metabolisms are related to the effect of FGF23 and its excess or deficiency leads to various hereditary diseases. Multiple studies have shown that FGF23 level increases in the very early stages of chronic kidney disease CKD , and its concentration may also be highly associated with cardiac complications. The present review is limited to some of the most important aspects of calcium and phosphate metabolism.

Iumor

FGF23 action on organs other than kidney and parathyroid remain unstudied, with the exception of bone, mainly because current data support that FGF23, even at supraphysiological concentrations, likely has no effect without the presence of Klotho. Different forms of DMP1 play distinct roles in mineralization. Nature , 45—51 Bone 51 —8. If true, this also suggests that circulating phosphorus levels do not adequately reflect phosphorus balance and that serum phosphate is not the major regulator of FGF23, at least in CKD. The biological function of DMP1 in osteocyte maturation is mediated by its 57 kDa C-terminal fragment. PLoS One e The major function of 1,25 OH 2 D 3 in mineral metabolism is the stimulation of intestinal calcium and phosphorus absorption. Accepted : 30 November Klotho lacks a vitamin D independent physiological role in glucose homeostasis, bone turnover, and steady-state PTH secretion in vivo. J Clin Invest —8. Abstract Fibroblast growth factor FGF23 is a bone-derived hormone suppressing phosphate reabsorption and vitamin D hormone synthesis in the kidney. Komaba H, Fukagawa M. Immunohistochemical localization of Klotho protein in brain, kidney, and reproductive organs of mice.

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Reprints and permissions. Annual Review of Physiology. Download as PDF Printable version. Aberrant Phex function in osteoblasts and osteocytes alone underlies murine X-linked hypophosphatemia. A high phosphorus diet was shown to enhance, and a low phosphorus diet to inhibit, the elevation of serum FGF23 levels in nephrectomized rats, but this result was obtained after 4 wk of dietary treatment 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. Nature —4. Nonetheless, FGF23 is positively associated with left ventricular mass index and increased risk of having left ventricular hypertrophy 57 , 68 , , , FGF23 may also provide an explanation for the association between low bone remodeling and cardiovascular calcifications, since low osteocalcin expression, as a marker of bone turnover, is associated with high FGF23 and cardiovascular mortality The complete mammalian FGF family. Fgf23 and parathyroid hormone signaling interact in kidney and bone. Role of vitamin D metabolites in the prevention of the osteopenia induced by ovariectomy in the axial and appendicular skeleton of the rat. Physiological phosphate balance is of crucial biological importance to skeletal mineralization, and as a master regulator of phosphate homeostasis, FGF23 is bound to affect bone metabolism, cellular function, and mineralization. The kidney plays a central role in phosphate homeostasis.