Results 61 to 70 of about 232,776 (304)

Prognostic Importance of Fibroblast Growth Factor-23 in Dialysis Patients

open access: yesInternational Journal of Nephrology, 2014
Introduction. In this study, we aimed to demonstrate the correlation of FGF-23 levels with bone-mineral metabolism, anemia, and the treatment in dialysis patients. Methods.
Nilgül Akalin   +5 more
doaj   +1 more source

Is Fibroblast growth factor 23 the leading cause of increased mortality among chronic kidney disease patients? A narrative review

open access: yesJournal of Advanced Research, 2017
The death rate among chronic kidney disease patients is the highest compared to other chronic diseases. 60% of these fatalities are cardiovascular. Cardiovascular calcifications and chronic inflammation affect almost all chronic kidney disease patients ...
Usama A.A. Sharaf El Din   +2 more
doaj   +1 more source

Fibrous Dysplasia and Fibroblast Growth Factor-23 Regulation [PDF]

open access: yesCurrent Osteoporosis Reports, 2013
Fibrous dysplasia (FD) is a skeletal disorder caused by activating mutations in Gsα that result in elevations in cAMP. A feature of FD is elevated blood levels of the bone cell-derived phosphaturic hormone, fibroblast growth factor-23 (FGF23). FGF23 regulates serum phosphorus and active vitamin D levels by action on proximal renal tubule cells.
Alison M, Boyce   +2 more
openaire   +2 more sources

YAP1::TFE3 mediates endothelial‐to‐mesenchymal plasticity in epithelioid hemangioendothelioma

open access: yesMolecular Oncology, EarlyView.
The YAP1::TFE3 fusion protein drives endothelial‐to‐mesenchymal transition (EndMT) plasticity, resulting in the loss of endothelial characteristics and gain of mesenchymal‐like properties, including resistance to anoikis, increased migratory capacity, and loss of contact growth inhibition in endothelial cells.
Ant Murphy   +9 more
wiley   +1 more source

Induction of FGF23-related hypophosphatemic osteomalacia by alcohol consumption

open access: yesBone Reports, 2021
Context: Fibroblast growth factor (FGF) 23 is a hormone that regulates serum phosphate levels, the excess action of which causes chronic hypophosphatemic rickets/osteomalacia.
Naoko Hidaka   +9 more
doaj   +1 more source

Abstract #1595981: Changes in Fibroblast Growth Factor-23 and the Klotho Protein Axis in Diabetic Nephropathy [PDF]

open access: bronze, 2023
Nozimakhon Nazarova   +7 more
openalex   +1 more source

Fibroblast Growth Factor 23 and Inflammation in CKD [PDF]

open access: yesClinical Journal of the American Society of Nephrology, 2012
Summary Background and objectives Levels of fibroblast growth factor 23 (FGF23) and inflammatory markers are commonly elevated in CKD, and each is associated with adverse clinical outcomes. This study tested the hypothesis that FGF23 is independently associated with inflammation in CKD.
Jair, Munoz Mendoza   +14 more
openaire   +2 more sources

Emerging role of ARHGAP29 in melanoma cell phenotype switching

open access: yesMolecular Oncology, EarlyView.
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster   +3 more
wiley   +1 more source

Fibroblast Growth Factor 23: Mineral Metabolism and Beyond [PDF]

open access: yes, 2017
Patients affected by chronic kidney disease (CKD) exhibit a high risk of cardiovascular mortality that is poorly explained by traditional risk factors. There is a growing awareness about the role of derangement of mineral metabolism that is currently accepted as a trigger and sustainer of cardiovascular disease (CVD) in CKD patients.
Grabner, Alexander   +8 more
openaire   +2 more sources

Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids

open access: yesMolecular Oncology, EarlyView.
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici   +8 more
wiley   +1 more source

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