Download Fibroblast Growth Factor 23 Ebook PDF

Fibroblast Growth Factor 23

Fibroblast Growth Factor 23
A Book

by Christian Faul,Kenneth White,Orlando Gutierrez

  • Publisher : Elsevier
  • Release : 2021-04-06
  • Pages : 376
  • ISBN : 0128180374
  • Language : En, Es, Fr & De
GET BOOK

Fibroblast Growth Factor 23 describes how FGF23 was initially identified as a bone-derived factor targeting the kidney. As such, sections in this comprehensive book cover exciting research that shows that different FGF23 effects require distinct signaling receptors and mediators that differ among target tissues, cover FGF23 initially identified as a bone-derived factor targeting the kidney, look at FGF23 as a regulator of phosphate metabolism and beyond, and cover research on novel concepts of FGF receptor signaling. Additional sections cover biochemistry, pharmacology and nephrology, making this book an ideal reference source on FGF23. Provides a comprehensive collection of chapters on the diversity of FGF23's actions Highlights truly translational topics, from molecular signaling to physiology and mechanism of disease, discussing cell culture and animal models to study FGF23 Describes FGF23’s potential in the clinical setting as a biomarker or even drug target Presents leaders in the field who cover a wide spectrum of research backgrounds and expertise, including clinical and basic scientists who specialize in diseases, endocrinology, genetics, protein biochemistry, cell biology and physiology

Fibroblast Growth Factor-23 in Canine Kidney Disease

Fibroblast Growth Factor-23 in Canine Kidney Disease
A Book

by Laura M. Harjes

  • Publisher : Unknown Publisher
  • Release : 2017
  • Pages : 39
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

Chronic kidney disease (CKD) is associated with hyperphosphatemia, reduced vitamin D metabolite concentrations, and hyperparathyroidism. This syndrome is known as CKD-mineral and bone disorder (CKD-MBD). Recently it has been shown that increased fibroblast growth factor-23 (FGF23) concentration is one of the earliest biomarkers of CKD in people and cats. It is an independent risk factor for both progression of kidney disease and survival time in humans and cats. FGF23 information in healthy and CKD dogs is lacking. The primary objective of this study was to measure FGF23 concentration in dogs with different stages of CKD and to determine its association with factors involved in CKD-MBD, including phosphate and parathyroid hormone (PTH) concentrations. A secondary aim was to validate an ELISA for measurement of canine plasma FGF23. Thirty-two client-owned dogs with naturally occurring CKD and 10 healthy control dogs were enrolled in this prospective cross-sectional study. A human FGF23 ELISA was used to measure plasma FGF23 and its association with creatinine, phosphate, calcium, and PTH was determined. Plasma FGF23 concentration increased with severity of kidney disease and was significantly different between IRIS stages 1 and 2 versus stages 3 and 4 (P

The Role of Circulating Fibroblast Growth Factor-23 (FGF-23) in Chronic Kidney Disease - Mineral Bone Disorder (CKB-MBD)

The Role of Circulating Fibroblast Growth Factor-23 (FGF-23) in Chronic Kidney Disease - Mineral Bone Disorder (CKB-MBD)
A Book

by Dr. Padmini Ajit Kumar Manghat,King's College London. Guy's, King's and St. Thomas's School of Medicine

  • Publisher : Unknown Publisher
  • Release : 2012
  • Pages : 292
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

Background and aim: Fibroblast Growth Factor-23 (FGF-23) has been shown to be elevated in early stage CKD. The primary stimulus for this increase remains unclear and it is still unknown whether the increase in FGF-23 has a biological effect on bone metabolism and vascular calcification. The aim of the study was to investigate in a cross - sectional design (1) the factors which are associated with elevated serum FGF-23 (2) the association between FGF-23 and bone metabolism (3) the association between FGF-23 and vascular stiffness in CKD. -- Method: One hundred and forty five ambulant predialysis patients (74 M, 71 F) aged (mean [SD]) 53 [14] years with CKD 1-4 were studied. Routine biochemical parameters were measured. In addition C - reactive protein (CRP), 1,25 dihydroxyvitamin D, FGF-23, bone turnover markers (bone alkaline phosphatase [BAP] and tartrate-resistant acid phosphatase [TRAP]) and the vascular calcification inhibitors, Matrix Gla Protein (MGP) and fetuin A were determined. HMD was measured at the lumbar spine, total hip, femoral neck and forearm. Arterial stiffness was assessed by contour analysis of digital volume pulse (SIovp)-Univariate and multiple linear regression analyses were undertaken. -- Results: FGF-23 was found to be elevated in CKD 3 compared to CKD 1, 2 although no significant differences in serum phosphate were observed. Serum phosphate (p

Endocrine and Paracrine Role of FGF23 and Klotho in Health and Disease

Endocrine and Paracrine Role of FGF23 and Klotho in Health and Disease
A Book

by Reinhold G. Erben,L. Darryl Quarles

  • Publisher : Frontiers Media SA
  • Release : 2019-04-05
  • Pages : 329
  • ISBN : 2889458059
  • Language : En, Es, Fr & De
GET BOOK

αKlotho and fibroblast growth factor-23 (FGF23) were discovered independently about 20 years ago. Since their initial description, a series of exciting discoveries have revealed the important role of endocrine and paracrine FGF23 and αKlotho signaling not only for the physiological regulation of mineral and bone homeostasis, but also for the pathophysiology of diseases such as chronic kidney disease, left ventricular hypertrophy, myocardial infarction, hypertension, and disorders characterized by impaired bone mineralization. The 11 articles compiled in this Research Topic consist of three Original Research articles and 8 Reviews or Mini Reviews, and are an excellent source of information about the state of the art in the FGF23/αKlotho field, covering almost all aspects of FGF23/αKlotho biology.

Fibroblast Growth Factor-23 as Novel Marker of Phosphate Homeostasis

Fibroblast Growth Factor-23 as Novel Marker of Phosphate Homeostasis
A Book

by Noreen Abbas,Aysha Habib Khan

  • Publisher : LAP Lambert Academic Publishing
  • Release : 2015-12-10
  • Pages : 96
  • ISBN : 9783659815126
  • Language : En, Es, Fr & De
GET BOOK

Fibroblast growth factor 23 (FGF-23), is recently discovered phosphaturic substance. It releases from bone osteocytes and plays a key role in the physiological regulation of phosphate metabolism. Excessive action of FGF23 results in several hypophosphatemic diseases characterized by impaired renal tubular phosphate reabsorption. In contrast, deficient action of FGF23 causes familial hyperphosphatemic tumoral calcinosis with enhanced renal tubular phosphate reabsorption. We carried out this study to gain knowledge about the current status of FGF-23 levels in our population and its relationship with serum phosphate; TmP/GFR and dietary phosphate; which has implications for the diagnosis and treatment of phosphate-wasting disorders and may guide us in planning further studies to see its role and implications on vitamin D metabolism.

Fibroblast Growth Factor 23 Induces Left Ventricular Hypertrophy

Fibroblast Growth Factor 23 Induces Left Ventricular Hypertrophy
A Book

by Ansel Philip Amaral

  • Publisher : Unknown Publisher
  • Release : 2012
  • Pages : 329
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

Over one in ten adults manifests physiological evidence of chronic kidney disease (CKD), which significantly reduces life expectancy due to cardiovascular complications. Left ventricular hypertrophy (LVH) is at the center of this relationship and up to 90% of patients with CKD also manifest LVH. Fibroblast growth factor (FGF) 23 is a phosphorus-regulating hormone responsible for maintaining normal serum phosphate levels in early stages of CKD; furthermore, FGF23 levels rise during the course of the disease and correlate with the CKD stage. High plasma FGF23 levels are independently associated with elevated left ventricular mass, LVH and increased risk of mortality. These correlative data suggest a direct role of FGF23 in the pathogenesis of cardiovascular disease; however, a direct causal mechanism of FGF23-induced LVH and subsequent death has yet to be demonstrated. This thesis project explores the direct effects of FGF23 on the heart. Our results indicate that FGF23 can activate pro-hypertrophic gene programs, elevate the expression levels of sarcomeric proteins and cause an increase in cardiac myocyte surface area. Cardiac elevation of FGF23 levels via intramyocardial injection induce hypertrophy in vivo. Furthermore, systemic elevation of serum FGF23 levels in mice via tail-vein injections results in a hypertrophic cardiac phenotype when compared to PBS-injected control animals. We show that FGF23- mediated signaling in cardiac myocytes occurs in an FGF receptor-dependent manner, but in the absence of klotho, a previously described co-receptor required for FGF23's biological effects in the kidney and parathyroid glands. Homozygous klotho-ablated mice, which have a greater than 15-fold increase in serum FGF23 levels compared to wild-type littermate controls, develop LVH. Interestingly, heterozygous klotho-ablated mice display a 4-fold increase in serum FGF23 and subsequently develop a moderate cardiac hypertrophic phenotype. Serum FGF23 levels are 12-fold increased in 5/6 nephrectomized rats compared to sham controls, and treatment with a pan-FGF receptor inhibitor attenuates LVH despite no change in blood pressure or kidney parameters. In dissecting the pathways responsible for FGF23-induced cardiac hypertrophy, our results indicate that the effect of FGF23 on cardiac myocytes is largely mediated through a calcineurin-dependent pathway, ultimately resulting in the activation of nuclear factor of activated T cells (NFAT). Our future research endeavors will continue to focus on the signaling events responsible for FGF23-mediated hypertrophy, with the ultimate goal of identifying the cardiac FGF23 receptor(s) involved in initiating this pro-hypertrophic signaling cascade and suggesting a plausible therapeutic intervention for preventing the high rates of LVH found in the CKD population.

Fibroblast Growth Factor 23: a Bridge Between Bone Minerals and Renal Volume Handling

Fibroblast Growth Factor 23: a Bridge Between Bone Minerals and Renal Volume Handling
A Book

by Jelmer Kor Humalda

  • Publisher : Unknown Publisher
  • Release : 2016
  • Pages : 329
  • ISBN : 9789036791908
  • Language : En, Es, Fr & De
GET BOOK

Studies on the Regulation of the Phosphaturic Hormone Fibroblast Growth Factor 23 (FGF23)

Studies on the Regulation of the Phosphaturic Hormone Fibroblast Growth Factor 23 (FGF23)
A Book

by Ludmilla Bär

  • Publisher : Unknown Publisher
  • Release : 2019
  • Pages : 329
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

Fibroblast Growth Factor 23 and Sudden Versus Non-sudden Cardiac Death

Fibroblast Growth Factor 23 and Sudden Versus Non-sudden Cardiac Death
The Cardiovascular Health Study

by Anonim

  • Publisher : Unknown Publisher
  • Release : 2015
  • Pages : 7
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

BACKGROUND: Elevated fibroblast growth factor 23 (FGF-23) concentrations are associated with greater risk of cardiovascular events and mortality, especially among people with chronic kidney disease (CKD). Because individuals with CKD are at an increased risk of sudden cardiac death (SCD), we sought to understand whether FGF-23 level is a stronger risk factor for SCD versus non-SCD. STUDY DESIGN: Cohort study. SETTING & PARTICIPANTS: 3,244 participants 65 years or older in the community-based Cardiovascular Health Study. PREDICTOR: Plasma FGF-23 concentrations. OUTCOMES: We assessed SCD and non-SCD in these analyses. SCD was adjudicated rigorously and was defined as a sudden pulseless condition of cardiac origin in a previously stable person occurring out of hospital or in the emergency department. MEASUREMENTS: We estimated associations of baseline FGF-23 concentrations with SCD and non-SCD using Cox proportional hazards models after adjustment for demographics, cardiovascular risk factors, comorbid conditions, and kidney function. We also tested whether associations differed by CKD status. RESULTS: During a median follow-up of 8.1 years, there were 118 adjudicated SCD and 570 non-SCD events. After multivariable adjustment for demographics, cardiovascular risk factors, comorbid conditions, and parameters of kidney function, higher FGF-23 concentrations were an independent risk factor for non-SCD (HR [per doubling], 1.17; 95% CI, 1.06-1.30). However, elevated FGF-23 concentrations were not associated independently with SCD (HR [per doubling], 1.07; 95% CI, 0.85-1.35). In stratified analysis by CKD status (36.5% of cohort), doubling of FGF-23 concentrations was associated independently with non-SCD (adjusted HR, 1.26; 95% CI, 1.10-1.45). A similar magnitude of association was observed between FGF-23 level and SCD in the CKD subgroup; however, it was not significant (HR, 1.20; 95% CI, 0.89-1.62). LIMITATIONS: Limited power to detect moderate-sized effects between FGF-23 level and SCD in both the primary and stratified analyses. CONCLUSIONS: In this population-based study, FGF-23 level elevations were associated independently with non-SCD. Among individuals with CKD, the associations between FGF-23 level and SCD and non-SCD were similar.

Phosphate and Vitamin D in Chronic Kidney Disease

Phosphate and Vitamin D in Chronic Kidney Disease
A Book

by M.S. Razzaque

  • Publisher : Karger Medical and Scientific Publishers
  • Release : 2013-05-02
  • Pages : 162
  • ISBN : 3318023698
  • Language : En, Es, Fr & De
GET BOOK

The enormous progress made during the last decade has resulted in a better conceptual understanding of mineral ion metabolism in general. With regard to chronic kidney disease, the two most affected nutrients are phosphate and vitamin D. This book provides an overview of the physiological aspects of phosphate and vitamin D metabolism, and how their pathological dysregulation facilitates advancement of chronic kidney disease. It looks into the complex molecular and organ cross-talks during disease progression that range from the involvement of fibroblast growth factor (FGF23)-klotho system to impaired phosphate transport to hormonal dysfunctions of PTH and vitamin D. Each chapter clearly presents the clinically and biologically important problems and lists the key unsolved issues related to chronic kidney disease and beyond. Illustrations explaining multi-factorial and multi-organ interactions provide an easy outline for the reader to appreciate the complex biological pathways. For those without prior familiarity with the subject matter, this volume may serve as a quick reference to get updated information on phosphate and vitamin D metabolism.

The Vitamin D – Fibroblast Growth Factor 23 – Klotho Axis and Progression of Chronic Kidney Disease

The Vitamin D – Fibroblast Growth Factor 23 – Klotho Axis and Progression of Chronic Kidney Disease
A Book

by Anonim

  • Publisher : Unknown Publisher
  • Release : 2017
  • Pages : 134
  • ISBN : 9789036794565
  • Language : En, Es, Fr & De
GET BOOK

Identification of Novel Regulators of Fibroblast Growth Factor 23 (FGF23) Production

Identification of Novel Regulators of Fibroblast Growth Factor 23 (FGF23) Production
The Role of High-fat Diet and AMP-activated Protein Kinase (AMPK) [kumulative Dissertation]

by Philipp Glosse

  • Publisher : Unknown Publisher
  • Release : 2020*
  • Pages : 329
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

FGF23; Klotho; kidney; calcium; phosphate; Orai1; inflammation; energy deficiency.

Endocrine FGFs and Klothos

Endocrine FGFs and Klothos
A Book

by Makoto Kuro-o

  • Publisher : Springer Science & Business Media
  • Release : 2012-03-06
  • Pages : 210
  • ISBN : 1461408873
  • Language : En, Es, Fr & De
GET BOOK

Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various metabolic processes in adulthood. Such FGFs, collectively called endocrine FGFs, are comprised of three members (FGF15/19, FGF21, and FGF23: FGF15 is the mouse ortholog of human FGF19). These endocrine FGFs share a common structural feature that enables the endocrine mode of action at the expense of the affinity to FGF receptors. To restore the affinity to FGF receptors in their target organs, the endocrine FGFs have designated the Klotho family of transmembrane proteins as obligate co-receptors. By expressing Klothos in a tissue-specific manner, this unique co-receptor system also enables the endocrine FGFs to specify their target organs among many tissues that express FGF receptors.

Fibroblast Growth Factor 23 Directly Targets Hepatocytes to Promote Inflammation in Chronic Kidney Disease

Fibroblast Growth Factor 23 Directly Targets Hepatocytes to Promote Inflammation in Chronic Kidney Disease
A Book

by Saurav Singh

  • Publisher : Unknown Publisher
  • Release : 2016
  • Pages : 329
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

Chronic kidney disease (CKD) is a global health problem that affects 10-15% of the adult population worldwide and significantly increases the risk of death. Patients with CKD develop marked elevations in circulating levels of the phosphaturic hormone, fibroblast growth factor 23 (FGF23), which correlate with the stage of disease, and are associated with higher risk of mortality. Chronic inflammation is a hallmark of CKD. Circulating levels of inflammatory cytokines, such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-[alpha] (TNF-[alpha]) are significantly elevated in CKD patients and increase with disease progression. This inflammatory burden has been suggested to be a significant contributor to the high mortality rate in CKD. Furthermore, recent clinical studies have demonstrated that in CKD elevated serum levels of FGF23 are independently associated with higher circulating levels of inflammatory cytokines, which can stimulate FGF23 production in osteocytes. These correlative studies suggest a causative role of FGF23 in the development of systemic inflammation in CKD; however, the sources of inflammation and precise molecular mechanisms underlying the pathological interrelationship between deterioration of renal function, elevated FGF23 production and amplification of the inflammatory state are unknown. This thesis project explores the direct effects of FGF23 on the liver. Our data indicate that FGF23 can directly stimulate hepatocytes to produce inflammatory cytokines in the absence of [alpha]- klotho, which is the FGF23 co-receptor in the kidney that is not expressed by hepatocytes. By activating FGF receptor isoform 4 (FGFR4), FGF23 stimulates phospholipase C[gamma] (PLC[gamma])/calcineurin/nuclear factor of activated T cells (NFAT) signaling in hepatocytes, which increases expression and secretion of inflammatory cytokines, including CRP. We show that the elevation of serum FGF23 levels increases hepatic and circulating levels of CRP in wild-type mice, but not in FGFR4 knockout mice. Furthermore, administration of an isoform-specific FGFR4 blocking antibody reduces hepatic and circulating levels of CRP in the 5/6 nephrectomy rat model of CKD. By demonstrating that FGF23 can directly stimulate hepatic secretion of inflammatory cytokines, our findings suggest a novel mechanism of chronic inflammation in patients with CKD. We postulate that FGFR4 blockade might have therapeutic anti-inflammatory effects in CKD.

The Regulation of Fibroblast Growth Factor 23 in Autosomal Dominant Polycystic Kidney Disease

The Regulation of Fibroblast Growth Factor 23 in Autosomal Dominant Polycystic Kidney Disease
A Book

by Daniela Spichtig

  • Publisher : Unknown Publisher
  • Release : 2015
  • Pages : 329
  • ISBN : 9876543210XXX
  • Language : En, Es, Fr & De
GET BOOK

The Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis

The Role of Fibroblast Growth Factor 23 in Phosphate Homeostasis
A Book

by Tobias Erik Martin Larsson

  • Publisher : Unknown Publisher
  • Release : 2004
  • Pages : 80
  • ISBN : 9789155460136
  • Language : En, Es, Fr & De
GET BOOK

Fibroblast Growth Factor 23 and Dietary Factors in Renal Disease

Fibroblast Growth Factor 23 and Dietary Factors in Renal Disease
A Book

by Anonim

  • Publisher : Unknown Publisher
  • Release : 2015
  • Pages : 329
  • ISBN : 9789036779692
  • Language : En, Es, Fr & De
GET BOOK

Hypophosphatemia: New Insights for the Healthcare Professional: 2011 Edition

Hypophosphatemia: New Insights for the Healthcare Professional: 2011 Edition
ScholarlyPaper

by Anonim

  • Publisher : ScholarlyEditions
  • Release : 2012-01-09
  • Pages : 16
  • ISBN : 1464919747
  • Language : En, Es, Fr & De
GET BOOK

Hypophosphatemia: New Insights for the Healthcare Professional: 2011 Edition is a ScholarlyPaper™ that delivers timely, authoritative, and intensively focused information about Hypophosphatemia in a compact format. The editors have built Hypophosphatemia: New Insights for the Healthcare Professional: 2011 Edition on the vast information databases of ScholarlyNews.™ You can expect the information about Hypophosphatemia in this eBook to be deeper than what you can access anywhere else, as well as consistently reliable, authoritative, informed, and relevant. The content of Hypophosphatemia: New Insights for the Healthcare Professional: 2011 Edition has been produced by the world’s leading scientists, engineers, analysts, research institutions, and companies. All of the content is from peer-reviewed sources, and all of it is written, assembled, and edited by the editors at ScholarlyEditions™ and available exclusively from us. You now have a source you can cite with authority, confidence, and credibility. More information is available at http://www.ScholarlyEditions.com/.

Dietary Phosphorus

Dietary Phosphorus
Health, Nutrition, and Regulatory Aspects

by Jaime Uribarri,Mona S Calvo

  • Publisher : CRC Press
  • Release : 2017-09-27
  • Pages : 372
  • ISBN : 1351645846
  • Language : En, Es, Fr & De
GET BOOK

Phosphorus is an essential nutrient that occurs in almost all foods and is important for many normal physiological functions. In a typical Western diet, it is not harmful, but does adversely affect tissues in the body when consumed in excess or deficiency. This book provides a comprehensive review of various aspects of phosphorus in relation to human nutritional needs. Sections cover phosphorus nutrition and dietary issues; health risks associated with excess phosphorus intake that exceeds requirements; phosphorus intake in populations at risk; regulatory challenges and policy approaches; and environmental impacts of phosphates in the modern food supply. This book challenges the long held ideas that high dietary phosphorus intake beyond nutritional requirements is safe and the natural supply of phosphorus critical to agricultural and human food production is endless. Controversy surrounds the claim that largely unrestricted use of phosphorus in all aspects of food production from farm to fork increases dietary phosphorus intake and irretrievable environmental loss, both of which harm human and environmental health. The book editors have joined together experts in basic, medical, environmental, nutritional, and food science to explore the validity of these claims of harm from high intakes and the unchecked use of phosphorus in the global food supply. Despite the essential need for adequate phosphorus over all stages of plant, animal and human life, the growing evidence points to a worldwide increase in dietary phosphorus intake far beyond nutrient requirements, significant association with chronic disease risk even when renal function is not compromised, and the increase in environmental loss with crop run-off, animal husbandry, and unretrieved phosphorus from human waste. This current evidence alludes to a depleted, unsustainable natural supply of phosphorus, hazardous environmental pollution of lakes and waterways, and significant increases in the risk of kidney, skeletal, and other serious illnesses in humans in the future if action is not taken now.

The Role of Fibroblast Growth Factor-23 in Chronic Kidney Disease-mineral and Bone Disorder

The Role of Fibroblast Growth Factor-23 in Chronic Kidney Disease-mineral and Bone Disorder
A Book

by Majd A. I. Mirza

  • Publisher : Unknown Publisher
  • Release : 2010
  • Pages : 83
  • ISBN : 9789155478834
  • Language : En, Es, Fr & De
GET BOOK