FGF23 is a hormone that appears as the core regulator of phosphate metabolism. Great deal of data has accumulated to demonstrate increased FGF23 secretion from the bone to compensate for even subtle increases in serum phosphorus long before intact PTH. However, recent evidence points to the fact that actions and interactions of FGF23 are not limited solely to phosphate metabolism. FGF23 may be implicated in iron metabolism and erythropoiesis, inflammation, insulin resistance, proteinuria, acute kidney injury and left ventricular hypertrophy. In this review, we will summarize latest experimental and clinical data examining impact of FGF23 on aforementioned pathophysiologic pathways/disorders.

Novel faces of fibroblast growth factor 23 (FGF23): iron deficiency, inflammation, insulin resistance, left ventricular hypertrophy, proteinuria and acute kidney injury / M. Kanbay, M. Vervloet, M. Cozzolino, D. Siriopol, A. Covic, D. Goldsmith, Y. Solak. - In: CALCIFIED TISSUE INTERNATIONAL. - ISSN 0171-967X. - (2016). [Epub ahead of print] [10.1007/s00223-016-0206-7]

Novel faces of fibroblast growth factor 23 (FGF23): iron deficiency, inflammation, insulin resistance, left ventricular hypertrophy, proteinuria and acute kidney injury

M. Cozzolino;
2016

Abstract

FGF23 is a hormone that appears as the core regulator of phosphate metabolism. Great deal of data has accumulated to demonstrate increased FGF23 secretion from the bone to compensate for even subtle increases in serum phosphorus long before intact PTH. However, recent evidence points to the fact that actions and interactions of FGF23 are not limited solely to phosphate metabolism. FGF23 may be implicated in iron metabolism and erythropoiesis, inflammation, insulin resistance, proteinuria, acute kidney injury and left ventricular hypertrophy. In this review, we will summarize latest experimental and clinical data examining impact of FGF23 on aforementioned pathophysiologic pathways/disorders.
Acute kidney injury; Fibroblast growth factor 23; Inflammation; Insulin resistance; Left ventricular hypertrophy; Proteinuria
Settore MED/14 - Nefrologia
2016
9-nov-2016
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/451005
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