Inhibition of fibroblast growth factor 23 (FGF23) signaling rescues renal anemia

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Fibroblast Growth Factor 23 (FGF23) and Disorders of Phosphate Metabolism

Derangements in serum phosphate level result in rickets/osteomalacia or ectopic calcification indicating that healthy people without these abnormalities maintain serum phosphate within certain ranges. These results indicate that there must be a regulatory mechanism of serum phosphate level. Fibroblast growth factor 23 (FGF23) was identified as the last member of FGF family. FGF23 is produced by...

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The role of fibroblast growth factor 23 in renal disease.

Activating mutations in the fibroblast growth factor 23 (FGF23) gene were identified as the cause of autosomal dominant hypophosphataemic rickets (ADHR) [1]. This secreted protein was later shown to play a role in both physiological and pathological phosphate handling. FGF23 may be the key pathogenetic molecule in three different diseases with hypophosphataemia and inappropriate regulation of v...

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Ablation of systemic phosphate-regulating gene fibroblast growth factor 23 (Fgf23) compromises the dentoalveolar complex.

Fibroblast growth factor-23 (FGF23) is a hormone that modulates circulating phosphate (P(i)) levels by controlling P(i) reabsorption from the kidneys. When FGF23 levels are deficient, as in tumoral calcinosis patients, hyperphosphatemia ensues. We show here in a murine model that Fgf23 ablation disrupted morphology and protein expression within the dentoalveolar complex. Ectopic matrix formatio...

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Fibroblast growth factor 23 (FGF23) and early chronic kidney disease in the elderly.

BACKGROUND Better biomarkers of CKD reflecting responses to decreased glomerular filtration rate (GFR) are needed. We determined the value of estimated GFR (eGFR) as a threshold for the increase of plasma cFGF23 (C-terminal) and intact fibroblast growth factor-23 (iFGF23) (intact) concentrations in the course of chronic kidney disease (CKD) and compared this eGFR value with values related to in...

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Sorafenib may induce hypophosphatemia through a fibroblast growth factor-23 (FGF23)-independent mechanism.

Sorafenib, a drug approved for the treatment of advanced renal cancer, inhibits RAF/MAPK pathway, vascular endothelial receptor-2 and -3, platelet-derived growth factor receptor-2 and -3, and c-Kit [1]. Hypophosphatemia is a common side-effect, occurring in 45% of patients [2]. This metabolic derangement is mostly asymptomatic, but the mechanisms involved are unclear [2]. The physiological bala...

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ژورنال

عنوان ژورنال: The FASEB Journal

سال: 2018

ISSN: 0892-6638,1530-6860

DOI: 10.1096/fj.201700667r