ReviewPediatric nephrology (Berlin, Germany)2010
FGF-23 in bone biology.
Review in Pediatric nephrology (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 51 citations in OpenAlex.
- Acute ketamine administration corrects abnormal inflammatory bone markers in major depressive disorder.Molecular psychiatry · 2018Trial
- Markers of bone metabolism are affected by renal function and growth hormone therapy in children with chronic kidney disease.PloS one · 2015Trial
- Bone: A Neglected Endocrine Organ?Journal of clinical medicine · 2024Review
- Pulp chamber features, prevalence of abscesses, disease severity, and PHEX mutation in X-linked hypophosphatemic rickets.Journal of bone and mineral metabolism · 2021Article
- Low bone mineral density due to secondary hyperparathyroidism in theFASEB bioAdvances · 2020Article
- Osteoimmunology: A Current Update of the Interplay Between Bone and the Immune System.Frontiers in immunology · 2020Review
- Assessment of the Concentration of Bone Metabolism Markers: Sclerostin and FGF-23 in Children with Idiopathic Nephrotic Syndrome Treated with Glucocorticosteroids.Disease markers · 2019Article
- The Biological Activities of Vitamin D and Its Receptor in Relation to Calcium and Bone Homeostasis, Cancer, Immune and Cardiovascular Systems, Skin Biology, and Oral Health.BioMed research international · 2018Review
- Hypophosphatemic rickets due to perturbations in renal tubular function.Pediatric nephrology (Berlin, Germany) · 2014Review
- Recent advances in the noninvasive diagnosis of renal osteodystrophy.Kidney international · 2013Review
- Update on tenofovir toxicity in the kidney.Pediatric nephrology (Berlin, Germany) · 2013Review
- Article
- Sclerostin alters serum vitamin D metabolite and fibroblast growth factor 23 concentrations and the urinary excretion of calcium.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Renal phosphate handling in Gitelman syndrome--the results of a case-control study.Pediatric nephrology (Berlin, Germany) · 2013Article
- Phosphate homeostasis and its role in bone health.Pediatric nephrology (Berlin, Germany) · 2012Review
- Vitamin D status in children with chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2012Article
- Fibroblast growth factor-23 helps explain the biphasic cardiovascular effects of vitamin D in chronic kidney disease.International journal of biological sciences · 2012Review
- Serum osteoprotegerin, RANKL and fibroblast growth factor-23 in children with chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2011Article
- [FGF23 and Klotho: the new cornerstones of phosphate/calcium metabolism].Archives de pediatrie : organe officiel de la Societe francaise de pediatrie · 2011Review
- Parathyroid hormone and growth in chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2011Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated that levels of fibroblast growth factor 23 (FGF-23), a key regulator of phosphorus and vitamin D metabolism, rise dramatically as renal function declines and may play a key initiating role in disordered mineral and bone metabolism in patients with chronic kidney disease (CKD). The physiologic importance of FGF-23 in mineral metabolism was first identified in human genetic and acquired rachitic diseases and further characterized in animal models. FGF-23 and its regulators, including phosphate regulating endopeptidase homolog, dentin matrix 1 (DMP1), and matrix extracellular phosphoglycoprotein, are made primarily in bone, specifically in osteocytes. Dysregulation of these proteins results in osteomalacia, implicating the osteocyte in the regulation of skeletal mineralization. Studies in pediatric patients with CKD, the majority of whom have altered skeletal mineralization in early stages of CKD, have demonstrated that skeletal expression of both FGF-23 and its regulator, DMP1, are increased in early stages of CKD and that expression of these proteins is associated with alterations in skeletal mineralization. Thus, dysregulation of osteocytic proteins occur very early in the course of CKD and appear to be central to altered bone and mineral metabolism in this patient population.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.