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Fibroblast growth factor 23

FGF23, fibroblast growth factor 23
The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities and are involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. The product of this gene inhibits renal tubular phosphate transport. This gene was identified by its mutations associated with autosomal dominant hypophosphatemic rickets (ADHR), an inherited phosphate wasting disorder. Abnormally high level expression of this gene was found in oncogenic hypophosphatemic osteomalacia (OHO), a phenotypically similar disease caused by abnormal phosphate metabolism. Mutations in this gene have also been shown to cause familial tumoral calcinosis with hyperphosphatemia. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Klotho, Parathyroid Hormone, HAD, AGE, CAN
Papers on FGF23
Early and sustained changes in bone metabolism after severe burn injury.
Muschitz et al., Vienna, Austria. In J Clin Endocrinol Metab, Feb 2016
During the early phase pronounced increases were observed for CTX, P1NP, sclerostin, DKK-1, BALP, FGF23 and iPTH levels, whereas 25-OH vitamin D, albumin, serum and ionized calcium levels decreased.
Pruning the ricket thicket.
Wolf et al., In J Clin Invest, Feb 2016
UNASSIGNED: Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by renal phosphate wasting, inappropriately low circulating levels of the active form of vitamin D, and skeletal abnormalities.
CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disorders.
Karaplis et al., In J Clin Invest, Feb 2016
Basal renal and extrarenal CYP24 is usually low but is highly induced by its substrate 1,25-dihydroxyvitamin D. Unbalanced high and/or long-lasting CYP24 expression has been proposed to underlie diseases like chronic kidney disease, cancers, and psoriasis that otherwise should favorably respond to supplemental vitamin D. Using genetically modified mice, we have shown that renal phosphate wasting hypophosphatemic states arising from high levels of fibroblast growth factor 23 (FGF23) are also associated with increased renal Cyp24 expression, suggesting that elevated CYP24 activity is pivotal to the pathophysiology of these disorders.
Therapeutic potential of the endocrine fibroblast growth factors FGF19, FGF21 and FGF23.
Moschetta et al., Bari, Italy. In Nat Rev Drug Discov, Jan 2016
The endocrine fibroblast growth factors (FGFs), FGF19, FGF21 and FGF23, are critical for maintaining whole-body homeostasis, with roles in bile acid, glucose and lipid metabolism, modulation of vitamin D and phosphate homeostasis and metabolic adaptation during fasting.
Mineral and bone disorder after kidney transplantation.
Disthabanchong et al., Bangkok, Thailand. In World J Transplant, Jan 2016
During the first 3 mo, fibroblast growth factor-23 (FGF-23) and parathyroid hormone levels decrease rapidly in association with an increase in 1,25-dihydroxyvitamin D production.
Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.
Faul et al., Miami, United States. In Cell Metab, Jan 2016
Here, we report that FGF23 exclusively activates FGFR4 on cardiac myocytes to stimulate phospholipase Cγ/calcineurin/nuclear factor of activated T cell signaling.
Serum Fibroblast Growth Factor 23 (FGF23) in Patients with Rheumatoid Arthritis.
Narita et al., Niigata, Japan. In Intern Med, Dec 2015
Fibroblast growth factor 23 (FGF23), which is mainly produced by osteocytes, circulates to the kidneys and regulates bone metabolism.
Tumour-induced osteomalacia: a literature review and a case report.
Kacergius et al., Vilnius, Lithuania. In World J Surg Oncol, Dec 2015
Mesenchymal tumour itself may be related to fibroblast growth factor 23 (FGF23), which is responsible for hypophosphataemia and phosphaturia occurring in this paraneoplastic syndrome.
Consequences of a high phosphorus intake on mineral metabolism and bone remodeling in dependence of calcium intake in healthy subjects - a randomized placebo-controlled human intervention study.
Glei et al., Jena, Germany. In Nutr J, Dec 2015
The main aims of the present study were to determine the influence of a high phosphorus intake in combination with different calcium supplies on phosphorus, calcium, magnesium and iron metabolism as well as fibroblast growth factor 23 (FGF23) concentrations within eight weeks of supplementation.
Phosphate as a cardiovascular risk factor: effects on vascular and endothelial function.
Jardine et al., Glasgow, United Kingdom. In Lancet, Mar 2015
The mechanism is poorly understood; it is unclear whether phosphate has direct effects or effects mediated via calcification or FGF23.
Bone development and mineral homeostasis in the fetus and neonate: roles of the calciotropic and phosphotropic hormones.
Kovacs, St. John's, Canada. In Physiol Rev, 2014
Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids.
The rachitic tooth.
Somerman et al., Bethesda, United States. In Endocr Rev, 2014
Here we discuss conditions fitting under the umbrella of rickets, which traditionally referred to skeletal disease associated with vitamin D deficiency but has been more recently expanded to include newly identified factors involved in endocrine regulation of vitamin D, phosphate, and calcium, including phosphate-regulating endopeptidase homolog, X-linked, fibroblast growth factor 23, and dentin matrix protein 1. Systemic mineral metabolism intersects with local regulation of mineralization, and factors including tissue nonspecific alkaline phosphatase are necessary for proper mineralization, where rickets can result from loss of activity of tissue nonspecific alkaline phosphatase.
Metabolic acidosis increases fibroblast growth factor 23 in neonatal mouse bone.
Bushinsky et al., Rochester, United States. In Am J Physiol Renal Physiol, 2012
Thus metabolic acidosis directly increases FGF23 RNA and protein in mouse bone
Mutational analysis of patients with FGF23-related hypophosphatemic rickets.
Fujita et al., Tokyo, Japan. In Eur J Endocrinol, 2012
Analysis of PHEX mRNA from peripheral blood would be appropriate for the first screening step in determining the etiology of FGF23-related hypophosphatemic rickets.
Fibroblast growth factor-23 and death, heart failure, and cardiovascular events in community-living individuals: CHS (Cardiovascular Health Study).
Shlipak et al., San Diego, United States. In J Am Coll Cardiol, 2012
independently associated with all-cause death and incident heart failure in community-living older persons
FGF23 and mineral metabolism, implications in CKD-MBD.
Almaden et al., In Nefrologia, 2012
FGF23 produced by bone plays a role in regulating mineral metabolism. FGF23 is involved in mineral & bone metabolism disorders seen in chronic kidney disease. Review.
Inactivation of a novel FGF23 regulator, FAM20C, leads to hypophosphatemic rickets in mice.
Qin et al., Dallas, United States. In Plos Genet, 2011
Our findings indicate that FAM20C is essential to the differentiation of osteoblasts/osteocytes and is involved in the regulation of phosphate homeostasis via the mediation of FGF23
Phosphate and FGF-23.
Jüppner, Boston, United States. In Kidney Int, 2011
In human chronic kidney disease (CKD), plasma FGF-23 appears to be a sensitive biomarker of abnormal renal phosphate handling, as FGF-23 levels increase during early stages of kidney malfunction.
Phosphate and Klotho.
Kuro-O, Dallas, United States. In Kidney Int, 2011
Klotho is a putative aging suppressor gene encoding a single-pass transmembrane co-receptor that makes the fibroblast growth factor (FGF) receptor specific for FGF-23.
The intact nephron hypothesis: the concept and its implications for phosphate management in CKD-related mineral and bone disorder.
Slatopolsky, Saint Louis, United States. In Kidney Int, 2011
The same procedure also rapidly increases renal phosphate excretion independently of FGF-23, suggesting the possibility of an 'intestinal phosphatonin'.
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