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fibroblast growth factor 23

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https://www.readbyqxmd.com/read/28932769/microrna-expression-in-a-phosphaturic-mesenchymal-tumour
#1
Darrell Green, Irina Mohorianu, Isabelle Piec, Jeremy Turner, Clare Beadsmoore, Andoni Toms, Richard Ball, John Nolan, Iain McNamara, Tamas Dalmay, William D Fraser
Phosphaturic mesenchymal tumours are a heterogeneous set of bone and soft tissue neoplasms that can cause a number of paraneoplastic syndromes such as tumour induced osteomalacia. The term phosphaturic comes from the common finding that these tumours secrete high levels of fibroblast growth factor 23 which causes renal phosphate wasting leading to hypophosphatemia. Phosphaturic mesenchymal tumours are rare and diagnosis is difficult. A very active 68 year old male presented with bone pain and muscle weakness...
December 2017: Bone Reports
https://www.readbyqxmd.com/read/28926112/chronic-kidney-disease-and-vitamin-d-metabolism-in-human-bone-marrow-derived-mscs
#2
REVIEW
Shuanhu Zhou, Julie Glowacki
Vitamin D that is synthesized in the skin or is ingested undergoes sequential steps of metabolic activation via a cascade of cytochrome P450 enzymatic hydroxylations in the liver and kidney to produce 1α,25-dihydroxyvitamin D (1α,25(OH)2 D). There are many tissues that are able to synthesize 1α,25(OH)2 D, but the biological significance of extrarenal hydroxylases is unresolved. Human marrow-derived mesenchymal stem cells (marrow stromal cells, hMSCs) give rise to osteoblasts, and their differentiation is stimulated by 1α,25(OH)2 D...
August 2017: Annals of the New York Academy of Sciences
https://www.readbyqxmd.com/read/28926103/fam20c-regulates-osteoblast-behaviors-and-intracellular-signaling-pathways-in-a-cell-autonomous-manner
#3
Chao Liu, Hua Zhang, Priyam Jani, Xiaofang Wang, Yongbo Lu, Nan Li, Jing Xiao, Chunlin Qin
Recent studies indicate that Family with sequence similarity 20 member C (FAM20C) catalyzes the phosphorylation of secreted proteins, and participates in a variety of biological processes, including cell proliferation, migration, mineralization and phosphate homeostasis. To explore the local influences of FAM20C on osteoblast, Fam20c-deficient osteoblasts were generated by treating the immortalized Fam20c(f/f) osteoblasts with CMV-Cre-IRES-EGFP lentivirus. Compared with the normal Fam20c(f/f) osteoblasts, the expression of Bone sialoprotein (Bsp), Osteocalcin (Ocn), Fibroblast growth factor 23 (Fgf23) and transcription factors that promote osteoblast maturation were up-regulated in the Fam20c-deficient osteoblasts...
September 19, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28924605/pai-1-is-a-critical-regulator-of-fgf23-homeostasis
#4
Mesut Eren, Aaron T Place, Paul M Thomas, Panagiotis Flevaris, Toshio Miyata, Douglas E Vaughan
Elevated levels of fibroblast growth factor 23 (FGF23), a bone-derived phosphaturic hormone, are associated with a number of pathologic conditions including chronic kidney disease, cardiac hypertrophy, and congestive heart failure. Currently, there are no specific treatments available to lower plasma FGF23 levels. We have recently reported that genetic plasminogen activator inhibitor-1 (PAI-1) deficiency provided a significant reduction in circulating FGF23 levels while simultaneously prolonging the life span of Klotho-deficient mice...
September 2017: Science Advances
https://www.readbyqxmd.com/read/28919046/fgf23-activates-injury-primed-renal-fibroblasts-via-fgfr4-dependent-signalling-and-enhancement-of-tgf-%C3%AE-autoinduction
#5
Edward R Smith, Stephen G Holt, Tim D Hewitson
Bone-derived fibroblast growth factor 23 (FGF23) is an important endocrine regulator of mineral homeostasis with effects transduced by cognate FGF receptor (FGFR)1-α-Klotho complexes. Circulating FGF23 levels rise precipitously in patients with kidney disease and portend to worse renal and cardiovascular outcomes. De novo expression of FGF23 has been found in the heart and kidney following injury but its significance remains unclear. Studies showing that exposure to chronically high FGF23 concentrations activates hypertrophic gene programmes in the cardiomyocyte, has spawned intense interest in other pathological off-target effects of FGF23 excess...
September 14, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28910790/the-cardiovascular-burden-in-end-stage-renal-disease
#6
Mario Cozzolino, Andrea Galassi, Francesca Pivari, Paola Ciceri, Ferruccio Conte
It is well documented that chronic kidney disease patients have an extremely high risk of developing cardiovascular (CV) disease (CVD) compared to the general population. Declining renal function itself represents a continuum of CV risk, and in those individuals who survive to reach end-stage renal disease, the risk of suffering a cardiac event is uncomfortably and unacceptably high. Several pathophysiological pathways have been suggested to account for this, including endothelial dysfunction, dyslipidemia, inflammation, left ventricular hypertrophy, troponins, phosphate, vitamin D, fibroblast growth factor-23, and NT-proBNP...
2017: Contributions to Nephrology
https://www.readbyqxmd.com/read/28910787/middle-molecule-uremic-toxins-and-outcomes-in-chronic-kidney-disease
#7
Ziad A Massy, Sophie Liabeuf
In patients with chronic kidney disease (CKD), uremic toxins constitute a specific nontraditional risk factor. Research in this field started in the early 1990s, and a growing body of preclinical and epidemiological evidence suggests that elevated levels of uremic toxins are associated with poor outcomes in a CKD setting. The present review focuses on a specific class of uremic toxins (the "middle molecules"), which includes well-known candidates like beta-2 microglobulin and fibroblast growth factor 23. Here, we summarize the epidemiological evidence linking the middle-molecule uremic toxin (and especially the larger ones) with hard clinical end points...
2017: Contributions to Nephrology
https://www.readbyqxmd.com/read/28900153/genetic-ablation-of-fgf23-or-klotho-does-not-modulate-experimental-heart-hypertrophy-induced-by-pressure-overload
#8
Svetlana Slavic, Kristopher Ford, Magalie Modert, Amarela Becirovic, Stephan Handschuh, Andreas Baierl, Nejla Katica, Ute Zeitz, Reinhold G Erben, Olena Andrukhova
Left ventricular hypertrophy (LVH) ultimately leads to heart failure in conditions of increased cardiac pre- or afterload. The bone-derived phosphaturic and sodium-conserving hormone fibroblast growth factor-23 (FGF23) and its co-receptor Klotho have been implicated in the development of uremic LVH. Using transverse aortic constriction (TAC) in gene-targeted mouse models, we examine the role of Fgf23 and Klotho in cardiac hypertrophy and dysfunction induced by pressure overload. TAC profoundly increases serum intact Fgf23 due to increased cardiac and bony Fgf23 transcription and downregulation of Fgf23 cleavage...
September 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28887454/the-intestinal-phosphate-transporter-napi-iib-slc34a2-is-required-to-protect-bone-during-dietary-phosphate-restriction
#9
Thomas Knöpfel, Eva M Pastor-Arroyo, Udo Schnitzbauer, Denise V Kratschmar, Alex Odermatt, Giovanni Pellegrini, Nati Hernando, Carsten A Wagner
NaPi-IIb/Slc34a2 is a Na(+)-dependent phosphate transporter that accounts for the majority of active phosphate transport into intestinal epithelial cells. Its abundance is regulated by dietary phosphate, being high during dietary phosphate restriction. Intestinal ablation of NaPi-IIb in mice leads to increased fecal excretion of phosphate, which is compensated by enhanced renal reabsorption. Here we compared the adaptation to dietary phosphate of wild type (WT) and NaPi-IIb(-/-) mice. High phosphate diet (HPD) increased fecal and urinary excretion of phosphate in both groups, though NaPi-IIb(-/-) mice still showed lower urinary excretion than WT...
September 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28877877/acute-blood-loss-stimulates-fibroblast-growth-factor-23-production
#10
Seham Rabadi, Ikemesit Udo, David Evan Leaf, Sushrut Waikar, Marta Christov
Fibroblast growth factor 23 (FGF23) production is upregulated by iron deficiency and hypoxia. However, the influence of acute blood loss, and the resulting increases in circulating erythropoietin, on FGF23 production is unknown. Using wild-type C57BL/6 mice, we show that acute loss of 10% total blood volume leads to an increase in plasma C-terminal FGF23 (cFGF23) levels within six hours, while plasma levels of intact FGF23, phosphate, calcium, parathyroid hormone, iron, and ferritin remain similar to control mice without acute blood loss...
September 6, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28870151/progression-of-arterial-stiffness-is-associated-with-changes-in-bone-mineral-markers-in-advanced-ckd
#11
Rathika Krishnasamy, Sven-Jean Tan, Carmel M Hawley, David W Johnson, Tony Stanton, Kevin Lee, David W Mudge, Scott Campbell, Grahame J Elder, Nigel D Toussaint, Nicole M Isbel
BACKGROUND: Arterial stiffness is an independent predictor of all-cause and cardiovascular mortality in patients with chronic kidney disease (CKD). There are limited prospective data however on progression of arterial stiffness in CKD, including evaluating associations with bone mineral markers such as fibroblast growth factor 23 (FGF23) and soluble α-klotho (sKl). METHODS: In this prospective, single-center, observational study, arterial stiffness [measured by pulse wave velocity (PWV)] and hormones influencing mineral homeostasis, including serum FGF23 and sKl, were compared between non-dialysis CKD stages 4/5 and healthy controls at baseline and 12 months (12 m)...
September 4, 2017: BMC Nephrology
https://www.readbyqxmd.com/read/28867373/etelcalcetide-amg-416-a-peptide-agonist-of-the-calcium-sensing-receptor-preserved-cortical-bone-structure-and-bone-strength-in-subtotal-nephrectomized-rats-with-established-secondary-hyperparathyroidism
#12
Xiaodong Li, Longchuan Yu, Frank Asuncion, Mario Grisanti, Shawn Alexander, Kelly Hensley, Chun-Ya Han, Qing-Tian Niu, Denise Dwyer, Kelly Villasenor, Marina Stolina, Charles Dean, Michael S Ominsky, Hua Zhu Ke, James E Tomlinson, William G Richards
Sustained elevation of parathyroid hormone (PTH) is catabolic to cortical bone, as evidenced by deterioration in bone structure (cortical porosity), and is a major factor for increased fracture risk in chronic kidney disease (CKD). Etelcalcetide (AMG 416), a novel peptide agonist of the calcium-sensing receptor, reduces PTH levels in subtotal nephrectomized (Nx) rats and in hemodialysis patients with secondary hyperparathyroidism (SHPT) in clinical studies; however, effects of etelcalcetide on bone have not been determined...
September 1, 2017: Bone
https://www.readbyqxmd.com/read/28860784/effect-of-additive-calcium-administration-on-fgf23-levels-in-patients-with-mild-chronic-kidney-disease-treated-with-calcitriol-a-randomized-open-labeled-clinical-trial
#13
Nayoung Han, Su Hyun Hong, Yon Su Kim, Dong Ki Kim, In-Wha Kim, Eunhee Ji, Jung Mi Oh
BACKGROUND: The purpose of the present study was to determine the effect of additional calcium carbonate treatment on fibroblast growth factor 23 (FGF23) levels in patients treated with calcitriol. METHODS: In this randomized, open-labeled, and parallel-group study, a total of 30 patients with early chronic kidney disease (CKD) and vitamin D deficiency were randomly assigned to two groups and received interventions for 8 weeks: 1) a combination of calcium carbonate and calcitriol group; and 2) calcitriol only group...
2017: Therapeutics and Clinical Risk Management
https://www.readbyqxmd.com/read/28859264/adefovir-induced-fanconi-syndrome-associated-with-osteomalacia
#14
Samel Park, Woo-Il Kim, Dai-Hyun Cho, Yeo-Joo Kim, Hong-Soo Kim, Ji-Hee Kim, Seung-Kuy Cha, Kyu-Sang Park, Ji-Hye Lee, Sang Mi Lee, Eun Young Lee
Fanconi syndrome is a dysfunction of the proximal renal tubules that results in impaired reabsorption and increased urinary loss of phosphate and other solutes. The pathophysiology of drug-induced Fanconi syndrome is unclear. Here we report the case of a 36-year-old woman who presented with pain in multiple bones and proteinuria. She had a 7-year history of taking adefovir at 10 mg/day for chronic hepatitis B. Three years previously she had received surgery for a nontraumatic right femur neck fracture, after which she continued to complain of pain in multiple bones, and proteinuria, glycosuria, and phosphaturia were noted...
September 1, 2017: Clinical and Molecular Hepatology
https://www.readbyqxmd.com/read/28852641/is-there-any-link-between-tumor-induced-osteomalacia-and-psoriasis-a-case-report
#15
Mojtaba Akbari, Bagher Larijani, Sasan Sharghi, Ali Jalili, Sayed Mahmoud Sajjadi-Jazi
BACKGROUND: Tumor-induced osteomalacia is an uncommon paraneoplastic syndrome caused by Fibroblast growth factor-23-secreting tumors. It is characterized by phosphaturia, hypophosphatemia, and a high plasma level of alkaline phosphatase. CASE PRESENTATION: We report a young patient with psoriasis who had suffered from bone pain and muscle weakness for more than 6.5 years. He was finally diagnosed with tumor-induced osteomalacia. However, mistakenly attributing the patient's signs and symptoms to psoriatic arthritis for a long time had resulted in multiple complications for the patient...
2017: Journal of Diabetes and Metabolic Disorders
https://www.readbyqxmd.com/read/28846459/calcifediol-to-treat-secondary-hyperparathyroidism-in-patients-with-chronic-kidney-disease
#16
Andrea Galassi, Antonio Bellasi, Paola Ciceri, Francesca Pivari, Ferruccio Conte, Mario Cozzolino
Deranged vitamin D metabolism represents an active trigger of secondary hyperparathyroidism (SHPT) in CKD. Correction of 25(OH)D deficiency by nutritional Vitamin D administration is suggested by KDIGO guidelines, to prevent and treat SHPT in CKD stage G3-G5 and G1T-G5T patients, although with a still inconsistent background. Nutritional vitamin D is available as cholecalciferol, ergocalciferol, or calcifediol. Superiority of calcifediol in increasing 25(OH)D levels has been suggested due to its better bioavailability...
August 28, 2017: Expert Review of Clinical Pharmacology
https://www.readbyqxmd.com/read/28843519/microrna-profiles-of-fibroblasts-derived-from-in-vivo-fertilized-and-fat-1-transgenic-cattle
#17
Yang Lv, Yu Wang, Jiajia Sun, Chunling Gong, Yan Chen, Guanghua Su, Guangqi Gao, Chunling Bai, Zhuying Wei, Lisheng Zhang, Shorgan Bou, Guangpeng Li
Fat-1 transgenic cattle have high levels of ω-3 fatty acids, which regulate several genes in fatty acid metabolism. In the current study, fibroblasts derived from in vivo fertilized (Ferti) and fat-1 transgenic (TG) Luxi cattle (Bos taurus), a local breed in China, were cultured and their miRNA expression was characterized. Expression of 352 known miRNAs differed in cells from Ferti and TG cattle: 83 miRNAs were found to be specifically expressed in cells from Ferti cattle while 23 miRNAs were found to be specifically expressed in cells from TG cattle...
August 23, 2017: Gene
https://www.readbyqxmd.com/read/28838895/associations-of-fibroblast-growth-factor-23-vitamin-d-and-parathyroid-hormone-with-5-year-outcomes-in-a-prospective-primary-care-cohort-of-people-with-chronic-kidney-disease-stage-3
#18
Adam Shardlow, Natasha J McIntyre, Richard J Fluck, Christopher W McIntyre, Maarten W Taal
OBJECTIVES: Vitamin D deficiency, elevated fibroblast growth factor 23 (FGF23) and elevated parathyroid hormone (PTH) have each been associated with increased mortality in people with chronic kidney disease (CKD). Previous studies have focused on the effects of FGF23 in relatively advanced CKD. This study aims to assess whether FGF23 is similarly a risk factor in people with early CKD, and how this risk compares to that associated with vitamin D deficiency or elevated PTH. DESIGN: Prospective cohort study...
August 23, 2017: BMJ Open
https://www.readbyqxmd.com/read/28834363/decreased-expression-of-thrombomodulin-in-endothelial-cells-by-fibroblast-growth-factor-23-%C3%AE-klotho
#19
Kenji Tanaka, Tancharoen Salunya, Yoshihiro Motomiya, Yasuki Motomiya, Yoko Oyama, Munekazu Yamakuchi, Ikuro Maruyama
Chronic kidney disease (CKD) has been known to be a state of excessive fibroblast growth factor-23 (FGF23) and α-Klotho deficiency. Patients undergoing hemodialysis have an increased mortality risk associated with cardiovascular disease and endothelial dysfunction. The mechanism responsible for the relationship of FGF23 to endothelial damage in these patients has been unclear. On the other hands, increasing evidences have demonstrated that thrombomodulin (TM) plays an important role in the endothelial barrier...
August 2017: Therapeutic Apheresis and Dialysis
https://www.readbyqxmd.com/read/28828171/serum-stweak-and-fgf-23-levels-in-hemodialysis-and-renal-transplant-patients
#20
H Eskandari Naji, A Ghorbanihaghjo, H Argani, S Raeisi, J Safa, A H Alirezaei, N Rashtchizadeh
BACKGROUND: Kidney transplantation is the treatment of choice for patients with end-stage renal disease. OBJECTIVE: To evaluate the changes in serum soluble TNF-like weak inducer of apoptosis (sTWEAK) and fibroblast growth factor 23 (FGF-23) in hemodialysis (HD) patients and renal transplant recipients (RTR). METHODS: Serum samples were obtained from 30 patients on chronic HD, 30 RTRs, and 30 normal controls. Biochemical factors, sTWEAK, FGF-23, and interlukin-6 (IL-6) were measured by standard methods...
2017: International Journal of Organ Transplantation Medicine
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