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Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions

Nature reviews. Nephrology, 2023-03, Vol.19 (3), p.185-193

2023

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Excessive Osteocytic Fgf23 Secretion Contributes to Pyrophosphate Accumulation and Mineralization Defect in Hyp Mice

PLoS biology, 2016-04, Vol.14 (4), p.e1002427-e1002427

2016

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Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis

Proceedings of the National Academy of Sciences - PNAS, 2014-04, Vol.111 (15), p.5520-5525

2014

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Parathyroid hormone receptor signaling in osteocytes increases the expression of fibroblast growth factor-23 in vitro and in vivo

Bone (New York, N.Y.), 2011-10, Vol.49 (4), p.636-643

2011

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Osteocytic FGF23 and Its Kidney Function

Frontiers in endocrinology (Lausanne), 2020-08, Vol.11, p.592-592

2020

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Initial FGF23-Mediated Signaling Occurs in the Distal Convoluted Tubule

Journal of the American Society of Nephrology, 2009-05, Vol.20 (5), p.955-960

2009

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Osteocyte regulation of phosphate homeostasis and bone mineralization underlies the pathophysiology of the heritable disorders of rickets and osteomalacia

Bone (New York, N.Y.), 2013-06, Vol.54 (2), p.213-221

2013

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Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice

Proceedings of the National Academy of Sciences - PNAS, 2011-11, Vol.108 (46), p.E1146-E1155

2011

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Chronic Hyperphosphatemia and Vascular Calcification Are Reduced by Stable Delivery of Soluble Klotho

Journal of the American Society of Nephrology, 2017-04, Vol.28 (4), p.1162-1174

2017

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Conditional Deletion of Murine Fgf23: Interruption of the Normal Skeletal Responses to Phosphate Challenge and Rescue of Genetic Hypophosphatemia

Journal of bone and mineral research, 2016-06, Vol.31 (6), p.1247-1257

2016

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Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism

Nature genetics, 2006-11, Vol.38 (11), p.1310-1315

2006

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Age and sex effects on FGF23-mediated response to mild phosphate challenge

Bone (New York, N.Y.), 2021-05, Vol.146, p.115885-115885, Article 115885

2021

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Both enantiomers of β-aminoisobutyric acid BAIBA regulate Fgf23 via MRGPRD receptor by activating distinct signaling pathways in osteocytes

Cell reports (Cambridge), 2024-07, Vol.43 (7), p.114397, Article 114397

2024

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Neonatal Iron Deficiency Causes Abnormal Phosphate Metabolism by Elevating FGF23 in Normal and ADHR Mice

Journal of bone and mineral research, 2014-02, Vol.29 (2), p.361-369

2014

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Molecular Insights into the Klotho-Dependent, Endocrine Mode of Action of Fibroblast Growth Factor 19 Subfamily Members

Molecular and Cellular Biology, 2007-05, Vol.27 (9), p.3417-3428

2007

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Fibroblast Growth Factor 23 in Oncogenic Osteomalacia and X-Linked Hypophosphatemia

The New England journal of medicine, 2003-04, Vol.348 (17), p.1656-1663

2003

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Erythropoietin and a hypoxia‐inducible factor prolyl hydroxylase inhibitor (HIF‐PHDi) lowers FGF23 in a model of chronic kidney disease (CKD)

Physiological reports, 2020-06, Vol.8 (11), p.e14434-n/a

2020

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Coupling fibroblast growth factor 23 production and cleavage: iron deficiency, rickets, and kidney disease

Current opinion in nephrology and hypertension, 2014-07, Vol.23 (4), p.411-419

2014

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Generation of two multipotent mesenchymal progenitor cell lines capable of osteogenic, mature osteocyte, adipogenic, and chondrogenic differentiation

Scientific reports, 2021-11, Vol.11 (1), p.22593-22593, Article 22593

2021

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The Roles of Specific Genes Implicated as Circulating Factors Involved in Normal and Disordered Phosphate Homeostasis: Frizzled Related Protein-4, Matrix Extracellular Phosphoglycoprotein, and Fibroblast Growth Factor 23

Endocrine reviews, 2006-05, Vol.27 (3), p.221-241

2006

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Hyperphosphatemic familial tumoral calcinosis: Response to acetazolamide and postulated mechanisms

American journal of medical genetics. Part A, 2014-06, Vol.164A (6), p.1545-1549

2014

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FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

The Journal of clinical investigation, 2003-09, Vol.112 (5), p.683-692

2003

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Single cell cortical bone transcriptomics define novel osteolineage gene sets altered in chronic kidney disease

Frontiers in endocrinology (Lausanne), 2023-01, Vol.14, p.1063083-1063083

2023

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Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

Best practice & research. Clinical rheumatology, 2011-10, Vol.25 (5), p.735-747

2011

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The pathophysiology of early‐stage chronic kidney disease–mineral bone disorder (CKD‐MBD) and response to phosphate binders in the rat

Journal of bone and mineral research, 2011-11, Vol.26 (11), p.2672-2681

2011

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Regulation of FGF23 production and phosphate metabolism by bone-kidney interactions

Excessive Osteocytic Fgf23 Secretion Contributes to Pyrophosphate Accumulation and Mineralization Defect in Hyp Mice

Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis

Parathyroid hormone receptor signaling in osteocytes increases the expression of fibroblast growth factor-23 in vitro and in vivo

Osteocytic FGF23 and Its Kidney Function

Initial FGF23-Mediated Signaling Occurs in the Distal Convoluted Tubule

Osteocyte regulation of phosphate homeostasis and bone mineralization underlies the pathophysiology of the heritable disorders of rickets and osteomalacia

Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice

Chronic Hyperphosphatemia and Vascular Calcification Are Reduced by Stable Delivery of Soluble Klotho

Conditional Deletion of Murine Fgf23: Interruption of the Normal Skeletal Responses to Phosphate Challenge and Rescue of Genetic Hypophosphatemia

Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism

Age and sex effects on FGF23-mediated response to mild phosphate challenge

Both enantiomers of β-aminoisobutyric acid BAIBA regulate Fgf23 via MRGPRD receptor by activating distinct signaling pathways in osteocytes

Neonatal Iron Deficiency Causes Abnormal Phosphate Metabolism by Elevating FGF23 in Normal and ADHR Mice

Molecular Insights into the Klotho-Dependent, Endocrine Mode of Action of Fibroblast Growth Factor 19 Subfamily Members

Fibroblast Growth Factor 23 in Oncogenic Osteomalacia and X-Linked Hypophosphatemia

Erythropoietin and a hypoxia‐inducible factor prolyl hydroxylase inhibitor (HIF‐PHDi) lowers FGF23 in a model of chronic kidney disease (CKD)

Coupling fibroblast growth factor 23 production and cleavage: iron deficiency, rickets, and kidney disease

Generation of two multipotent mesenchymal progenitor cell lines capable of osteogenic, mature osteocyte, adipogenic, and chondrogenic differentiation

The Roles of Specific Genes Implicated as Circulating Factors Involved in Normal and Disordered Phosphate Homeostasis: Frizzled Related Protein-4, Matrix Extracellular Phosphoglycoprotein, and Fibroblast Growth Factor 23

Hyperphosphatemic familial tumoral calcinosis: Response to acetazolamide and postulated mechanisms

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

Single cell cortical bone transcriptomics define novel osteolineage gene sets altered in chronic kidney disease

Hyperphosphatemic familial tumoral calcinosis (FGF23, GALNT3 and αKlotho)

The pathophysiology of early‐stage chronic kidney disease–mineral bone disorder (CKD‐MBD) and response to phosphate binders in the rat

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