Fibroblast growth factor 23

A protein that is encoded by the FGF23 gene.

An endocrine hormone thjat regulated phosphorus metabolism.

It is is a member of the fibroblast growth factor (FGF) family which aids in phosphate and vitamin D metabolism and regulation.

A member of the fibroblast growth factor (FGF) family which is responsible for phosphate metabolism.

Chromosome 12 

FGF family members possess many mitogenic and cell survival activities.

FGF family members involved in a variety of biological processes including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion.

Its main function is regulation of phosphate concentration in plasma.

FGF23 is secreted by osteocytes in response to increased calcitriol. 

Inhibits renal tubular phosphate transport.

FGF23 acts on the kidneys, where it decreases a sodium-phosphate cotransporter in the proximal tubule.

A phosphaturic hormone, in that it inhibits renal reabsorption of phosphate in the kidney, mostly in the proximal convoluted tubule.

Thus, FGF23 decreases the reabsorption of calcium and increases excretion of phosphate. 

FGF23 is mostly expressed in bone and connective tissue.

Previously known as phosphatonin.

Inhibits 1-hydroxylase, which is responsible for the conversion of calcifediol to calcitriol the biologically active form of Vitamin D.

Located on chromosome 12 and is composed of three exons.

Levels increase as renal function declines.

Highest levels known to be present in patients with chronic kidney disease.

Levels of fibroblast growth factor 23 increase in chronic renal insufficiency as a response to maintain neutral phosphate balance and normal phosphate levels with renal imnpairment of phosphate excretion.

FGF23 may suppress 1-alpha-hydroxylase, reducing its ability to activate vitamin D and subsequently impairing calcium absorption.

Mutations render the protein resistant to proteolytic cleavage leads to increased activity of FGF23 and the renal phosphate loss found in the human disease autosomal dominant hypophosphatemic rickets.

May be produced by some types of tumors, causing tumor-induced osteomalacia.

Loss of FGF23 activity can to lead to increased phosphate levels and the clinical syndrome of familial tumor calcinosis.

Elevation of FGF 23 is an independent risk factor for ESRD in patients with relatively preserved kidney function and for mortality across the spectrum of chronic kidney disease (Isakova T et al).

FGF23 excess causes renal phosphate loss and is found in autosomal dominant hypophosphatemic rickets. 

FGF23 mutations resist proteolytic cleavage increasing its activity.

FGF23 is also overproduced by some types of tumors, causing tumor-induced osteomalacia, a paraneoplastic syndrome.

The  mutational loss of FGF23 activity leads to increased phosphate levels and the clinical syndrome of familial tumor calcinosis: autosomal dominant hypophosphatemic rickets.

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