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FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1 (show STC1 Proteins))modulates cation levels in trpm7 (show TRPM7 Proteins) mutants and in the wild type; levels of cations are restored to normal in trpm7 (show TRPM7 Proteins) mutants when stc1 (show STC1 Proteins) activity is blocked.
A statistically significant positive correlation was found between s-Klotho (show KL Proteins) and FGF23 (r=0.768; p=0.001), and between FGF23 levels and urinary albumin (show ALB Proteins) creatinine ratio (r=0.768; p=0.001).
There may be positive dose-response predictive effects of FGF23 on all-cause mortality, cardiovascular disease, and renal events in patients with chronic kidney disease.[meta-analysis]
Circulating FGF23 and inflammatory cytokines are correlated with varying levels of chronic kidney disease.
study indicated that serum FGF-23 level could be served as the utility in the early detection of women with low bone mass.
Newly diagnosed Lupus nephritis (LN) patients demonstrated elevated FGF23 levels that were positively correlated to urinary MCP1 (show CCL2 Proteins), independently of vitamin D levels and kidney function. If FGF23 may predict clinical outcomes in LN warrants further evaluation.
there is a strong relationship between iron and FGF23 physiology; C-terminal FGF23 may have a role in mortality in kidney transplant recipients
FGF23 counteracts osteogenic conversion of vascular smooth muscle cells as a part of a compensatory mechanism to mitigate vascular calcification
intact FGF23 from loss of function mutants bypasses the endoplasmic reticulum/Golgi quality control system to the circulation of hyperphosphatemic familial tumoral calcinosis patients by an unknown pathway.
AN69ST-continuous hemodiafiltration can be a novel FGF-23 lowering therapy for acute illnesses requiring acute blood purification.
FGF23 and its co-receptor klotho (show KL Proteins) play an important role in bone mineral and vitamin D metabolism. In chronic kidney disease, disturbances in bone metabolism increase cardiovascular risk. FGF23 levels are very high in chronic kidney disease and may contribute to vascular calcification and other cardiovascular problems. Review.
deleting FGF23 within early osteoblasts and osteocytes demonstrated that both cell types contribute to baseline circulating FGF23 concentrations, and that targeting osteoblasts/osteocytes for FGF23 production can modify systemic responses to changes in serum phosphate concentrations and rescue the Hyp (show PHEX Proteins) genetic syndrome
Thus, monotherapy with 1,25D improves growth, skeletal microarchitecture, and bone strength in the absence of phosphate supplementation despite enhancing FGF23 expression, demonstrating that 1,25D has direct beneficial effects on the skeleton in XLH (show PHEX Proteins), independent of its role in phosphate homeostasis
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4 (show FGFR4 Proteins)
Zinc13407541 also inhibited FGF-23 signaling in isolated renal tubules ex vivo and partially reversed the hypophosphatemic effects of excess FGF-23 in a mouse model. These chemical probes provide a platform to develop lead compounds to treat disorders caused by excess FGF-23.
FGF23 may be an important modulator of PTH (show PTH Proteins) signaling in bone and kidney.
EPO (show EPO Proteins) dependent regulation pathway of FGF23 gene expression
Klotho (show KL Proteins) in bone is crucial for inducing FGF23 production upon renal failure
dietary iron content and chronic kidney disease affected FGF23 production and metabolism
Dmp1 (show DMP1 Proteins) mutation creates a lower set point for extracellular phosphate and maintains it through the regulation of Fgf23 cleavage and expression
Although FGF23 is present in the fetal circulation at levels that may equal adult values, and there is robust expression of FGF23 target genes in placenta and fetal kidneys, FGF23 itself is not an important regulator of fetal phosphorous metabolism.
This gene encodes a member of the fibroblast growth factor family of proteins, which possess broad mitogenic and cell survival activities and are involved in a variety of biological processes. The product of this gene regulates phosphate homeostasis and transport in the kidney. The full-length, functional protein may be deactivated via cleavage into N-terminal and C-terminal chains. Mutation of this cleavage site causes autosomal dominant hypophosphatemic rickets (ADHR). Mutations in this gene are also associated with hyperphosphatemic familial tumoral calcinosis (HFTC).
fibroblast growth factor 23
, tumor-derived hypophosphatemia inducing factor