ReviewBone research2013
FGF23 and Phosphate Wasting Disorders.
Review in Bone research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Meta-analysis and systematic review: burosumab as a promising treatment for children with X-linked hypophosphatemia.Frontiers in endocrinology · 2024Pooled it
- Interim Analysis of a Phase 2 Open-Label Trial Assessing Burosumab Efficacy and Safety in Patients With Tumor-Induced Osteomalacia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Trial
- Fibroblast growth factor receptor signaling in maturing osteoblasts controls cell-matrix interactions critical for osteocyte survival.Bone research · 2026Article
- Review
- Importance of Recognizing Renal Tubular Disorders as a Cause of Bone Hypomineralization and Fractures in Adults.Diagnostics (Basel, Switzerland) · 2026Review
- Fibroblast Growth Factor Receptor Signaling in Maturing Osteoblasts Controls Cell-Matrix Interactions Critical for Osteocyte Survival.bioRxiv : the preprint server for biology · 2026Article
- X-Linked Hypophosphatemia: Role of Fibroblast Growth Factor 23 on Human Skeletal Muscle-Derived Cells.Calcified tissue international · 2025Article
- Impact of Somatic Development and Course of Osteogenesis Imperfecta on FGF23 Levels in Children.International journal of molecular sciences · 2025Article
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- Phosphaturic mesenchymal tumor withTherapeutic advances in medical oncology · 2024Article
- Iron-induced Hypophosphatemic Osteomalacia-An Atypical Case of Bilateral Femoral Stress Fractures.Journal of the American Academy of Orthopaedic Surgeons. Global research & reviews · 2023Article
- The Association between Admission Serum Phosphorus and Preoperative Deep Venous Thrombosis in Geriatric Hip Fracture: A Retrospective Study.Diagnostics (Basel, Switzerland) · 2023Article
- Peripheral actions and direct central-local communications of melanocortin 4 receptor signaling.Journal of sport and health science · 2023Review
- Elevated morbidity and mortality in patients with chronic idiopathic hypophosphatemia: a nationwide cohort study.Frontiers in endocrinology · 2023Article
- Whole exome sequencing identifies two novel variants in PHEX and DMP1 in Malaysian children with hypophosphatemic rickets.Italian journal of pediatrics · 2022Article
- A Novel Synonymous Variant of PHEX in a Patient with X-Linked Hypophosphatemia.Calcified tissue international · 2022Article
- Activation of RAAS Signaling Contributes to Hypertension in AgedBiomedicines · 2022Article
- The regulation of FGF23 under physiological and pathophysiological conditions.Pflugers Archiv : European journal of physiology · 2022Review
- Salivary phosphate as a biomarker for human diseases.FASEB bioAdvances · 2022Article
- An Expert Perspective on Phosphate Dysregulation With a Focus on Chronic Hypophosphatemia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A decade ago, only two hormones, parathyroid hormone and 1,25(OH)2D, were widely recognized to directly affect phosphate homeostasis. Since the discovery of fibroblast growth factor 23 (FGF23) in 2000 (1), our understanding of the mechanisms of phosphate homeostasis and of bone mineralization has grown exponentially. FGF23 is the link between intestine, bone, and kidney together in phosphate regulation. However, we still do not know the complex mechanism of phosphate homeostasis and bone mineralization. The physiological role of FGF23 is to regulate serum phosphate. Secreted mainly by osteocytes and osteoblasts in the skeleton (2,3), it modulates kidney handling of phosphate reabsorption and calcitriol production. Genetic and acquired abnormalities in FGF23 structure and metabolism cause conditions of either hyper-FGF23 or hypo-FGF23. Hyper-FGF23 is related to hypophosphatemia, while hypo-FGF23 is related to hyperphosphatemia. Both hyper-FGF23 and hypo-FGF23 are detrimental to humans. In this review, we will discuss the pathophysiology of FGF23 and hyper-FGF23 related renal phosphate wasting disorders (4).
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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.