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FGF23 functions as a hypocalcemic hormone in zebrafish.
This study showed that stanniocalcin 1 (stc1)modulates cation levels in trpm7 mutants and in the wild type; levels of cations are restored to normal in trpm7 mutants when stc1 activity is blocked.
High serum levels of osteopontin, stanniocalcin-1 and FGF 23 at the time of surgery are important prognostic factors in renal cell carcinoma
Plasma FGF23 levels were significantly elevated in chronic obstructive pulmonary disease patients.
investigated the changes in serum FGF23 levels in patients diagnosed with acute myocardial infarction
Patients with prediabetes have higher FGF23 levels and higher prevalence of vitamin D deficiency compared to normal glucose tolerance subjects. Elevated FGF23 levels seem to be correlated more to elevated fasting blood glucose levels than to insulin resistance state of the patients.
In urothelial carcinoma patients, serum FGF19 level was significantly lower, while FGF21 and FGF23 were significantly higher, than respective levels in healthy controls.
Elevated serum FGF23 levels are positively associated with all-cause mortality and cardiovascular events in hemodialysis patients, with a 14 or 39% increase in all-cause mortality and a 21% increased risk of cardiovascular events.
elevated serum FGF21 and FGF23 levels may be useful biomarkers for predicting kidney disease progression, especially in the early stages of Diabetic nephropathy
Cases of hyperphosphatemic familial tumoral calcinosis, secondary to fibroblast growth factor 23 gene mutation.
Data suggest a synergistic interaction of cardiovascular (CV) risk factors and fibroblast growth factor 23 (FGF23) as a potentially novel determinant of brain health.
Serum FGF23 levels were positively correlated with body fat parameters and obesity.
This study revealed a dysequilibrium of the PTH-FGF23-vitamin D axis in RRMS, with lower plasma PTH, higher plasma iFGF23 and a lower serum 1,25(OH)2D to 25OHD ratio in RRMS compared with healthy control subjects.
cFGF23 measurement may serve as a novel biomarker for incident acute kidney injury and death among critically ill patients
Levels of circulating FGF-23 but not sclerostin were related to Aortic Arch Calcification (AoAC) severity. Serum FGF-23 levels were independently associated with AoAC.
Our findings demonstrate that severely polycystic livers produce FGF23 and increase levels of circulating FGF23 in patients with autosomal polycystic kidney disease.
Increases in plasma erythropoietin and erythropoietin receptor activation are mechanisms implicated in the increase of plasma FGF23 in acute kidney injury.
The FGF23 increase related to acute kidney injury, especially in more severe stages and in patients without diuresis, is an independent risk factor for mortality.
In patients with Autosomal Dominant Polycystic Kidney Disease, as the disease stage advanced, serum FGF-23 levels increased while s-KL decreased. In ADPKD patients, the effect of serum FGF-23 on the development of AS and atherosclerosis in peripheral vessels is independent of s-KL.
In summary, our results suggest that FGF23 gene polymorphisms are associated with the risk of developing EH in Chinese Han population.
Although there are many studies suggesting the correlation between FGF23 and Insulin resistance (IR) in different populations, this study did not find any statistically significant relationship between IR and FGF23 levels in metabolic syndrome.
Data suggest that intact FGF23 level in plasma is independent predictor of cardiovascular death in patients with heart failure and provides added value to standard of care, natriuretic peptide (NT-proBNP) plasma level, for risk estimation. This study was conducted in Belgium. (FGF23 = fibroblast growth factor 23; NT-proBNP = aminoterminal pro-B-type natriuretic peptide)
this study shows that the microbiota through FGF23 regulates vitamin D metabolism
Despite the profound, aldosterone-mediated increase in circulating intact Fgf23 after TAC, our data do not support an essential role of Fgf23 or Klotho in the pathophysiology of pressure overload-induced cardiac hypertrophy.
Study in Ampkalpha1-knockout and wild-type mice revealed that knockout mice had a higher serum Fgf23 concentration compared to wild-type mice. AMPK activator down-regulated, whereas the AMPK inhibitor induced Fgf23 transcription. Thus, AMPK participates in the regulation of Fgf23.
both FGF23 and Fetuin-A are present and strictly linked to each other in MSCs with FGF23 driving Fetuin-A production. This mechanism suggests a role for these two proteins in the osteoblast differentiation.
Mouse model of acute kidney injury (AKI) has an increase in bone FGF23 mRNA expression and increase in serum FGF23 and IL-6. IL-6 knock-out mice fed an adenine diet to induce chronic kidney disease (CKD) failed to increase bone FGF23 mRNA and had a muted increase in serum FGF23 levels. IL-6 increases FGF23 transcription and contributes to the high levels of serum FGF23 in both acute and chronic kidney disease.
FGF23 production is rapidly increased after acute blood loss and that erythropoietin may be the mediator of this increase
Osteoarthropathy of HMW FGF2 Trangenic is at least partially due to FGF23-modulated Wnt/beta-catenin signaling in chondrocytes.
Although previous studies showed that increased circulating FGF23 and phosphate levels are associated with LVH, our results demonstrated that in XLH, high circulating levels of FGF23 in the setting of hypophosphatemia do not induce cardiac hypertrophy.
our data highlight a role of FGF23/FGFR4 signaling in the regulation of cardiac remodeling and function, and indicate that pharmacological interference with cardiac FGF23/FGFR4 signaling might protect from CKD- and age-related LVH.
the main physiological function of Klotho for mineral homeostasis in vivo is its role as co-receptor mediating Fgf23 action.
our study provided histological evidences that sclerostin tends to be secreted in osteocytes of remodeled mature bone, while FGF23 would be differently synthesized in osteoblasts and osteocytes according to the developmental stages
these results indicate that Nf1 deficiency in osteocytes dramatically increases FGF23 production and causes a mineralization defect (ie, hyperosteoidosis) via the alteration of calcium-phosphorus metabolism.
FGF23 promotes myocardial fibrosis and exacerbates diastolic dysfunction induced by myocardial infarction or ischemia/reperfusion , which is associated with the upregulation of active beta-catenin and TGF-beta
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 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, independent of its role in phosphate homeostasis
FGF23 augments pro-fibrotic signalling cascades in injury-primed renal fibroblasts via activation of FGFR4
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 signaling in bone and kidney.
EPO dependent regulation pathway of FGF23 gene expression
SNPs in FGF23 and TRAFD1 were significantly associated with the serum calcium/phosphorus ratio and serum phosphorus levels, respectively
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