Fgf23

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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.

Fgf23

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. Fibroblast growth factor is a 32 kDa glycoprotein mainly produced in bone by osteoblasts and osteocytes under physiological circumstances. 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. ARHR1 is caused by loss-of-function mutations in dentin matrix protein-1, which is required for normal mineralization of bone It is currently believed that the excessive osteocytic and osteoblastic FGF23 secretion in both diseases is either driven by the impaired mineralization of the extracellular matrix, which may be detected by matrix-embedded bone cells through a putative sensing mechanism that may involve FGF receptors 19 , 20 , or by an altered set point for phosphate sensing in bone cells 21 ,

Parathyroid hormone secretion and action: evidence for discrete receptors for the carboxyl-terminal region and related biological actions of carboxyl-terminal ligands, 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 Briefly, the principal function of the PTH-vitamin D axis is to maintain serum calcium levels in a narrow range by stimulating 1,dihydroxyvitamin D [1,25 OH 2 D] production and decreasing urinary calcium excretion by the kidney.

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

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.

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Therefore, FGF23 may be a physiological regulator of erythroid lineage commitment in the bone microenvironment. Matrix extracellular phosphoglycoprotein MEPE correlates with serum phosphorus prior to and during octreotide treatment and following excisional surgery in hypophosphatemic linear sebaceous nevus syndrome. Knothe Tate, M. No abstract available. Vice versa , a reduction in PTH signaling in human patients with hypoparathyroidism has been shown to induce partial resistance to the phosphaturic actions of FGF23 52 , Introduction 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. Conclusion The purpose of this mini-review is to highlight the current knowledge about the physiological functions of the bone-derived hormone FGF Conditional deletion of Fgfr1 in the proximal and distal tubule identifies distinct roles in phosphate and calcium transport. J Clin Invest — Fibroblast growth factor receptor-1 FGFR1 nuclear dynamics reveal a novel mechanism in transcription control.

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.

Best Pract Res Clin Rheumatol. As a result, the protein is not inactivated, and an increased amount of the full-length, active protein circulates in the bloodstream. Effect of fibroblast growth factor on phosphate transport in proximal tubules. PLoS One 9:e Osteocyte-specific deletion of Fgfr1 suppresses FGF Fibroblast growth factor may also have physiologically relevant functions in bone on bone mineralization and on hematopoiesis. This supports the hypothesis of secreted Klotho mediating some of the effects of FGF Aline Martin , Valentin David , and L. As a library, NLM provides access to scientific literature. 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. Molecular insights into the Klotho-dependent, endocrine mode of action of fibroblast growth factor 19 subfamily members. No use, distribution or reproduction is permitted which does not comply with these terms. Fibroblast growth factor 23 signaling in hippocampal cells: impact on neuronal morphology and synaptic density.