ReviewCurrent osteoporosis reports2013
Fibrous dysplasia and fibroblast growth factor-23 regulation.
Review in Current osteoporosis reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 42 citations in OpenAlex.
- Burosumab treatment for FGF23-related hypophosphatemia in a two-year-old girl with McCune-Albright syndrome.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2026Article
- Burosumab treatment of a child with McCune-Albright syndrome/polyostotic fibrous dysplasia: challenges and benefits.JBMR plus · 2025Article
- Article
- Monostotic fibrous dysplasia of jaw bones: a case series.BMC oral health · 2024Article
- PTHrP Modulates the Proliferation and Osteogenic Differentiation of Craniofacial Fibrous Dysplasia-Derived BMSCs.International journal of molecular sciences · 2023Article
- Burosumab treatment for fibrous dysplasia.Bone · 2021Article
- Renal Phosphate Handling: Independent Effects of Circulating FGF23, PTH, and Calcium.JBMR plus · 2021Article
- Fibrous Dysplasia/McCune-Albright Syndrome: A Rare, Mosaic Disease of Gα s Activation.Endocrine reviews · 2020Review
- When Low Bone Mineral Density and Fractures Is Not Osteoporosis.Current osteoporosis reports · 2019Review
- Oncogenic osteomalacia caused by a phosphaturic mesenchymal tumor of the femur: A case report.World journal of clinical cases · 2019Article
- Fibrous dysplasia of bone: craniofacial and dental implications.Oral diseases · 2017Review
- Fibrous Dysplasia Mimicking Malignancy on 68Ga-DOTATATE PET/CT.Clinical nuclear medicine · 2017Article
- Cutaneous skeletal hypophosphatemia syndrome: clinical spectrum, natural history, and treatment.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016Review
- Fibrous Dysplasia/McCune-Albright Syndrome: Clinical and Translational Perspectives.Current osteoporosis reports · 2016Review
- FGF-23 serum levels and bone histomorphometric results in adult patients with chronic kidney disease on dialysis.Clinical nephrology · 2014Article
- New technologies in oral radiology as a diagnostic aid for monostotic fibrous dysplasia: a review.Revista cientifica odontologica (Universidad Cientifica del Sur)Review
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 3 institutions in 1 country.
Funding
Abstract
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. An essential step in the production of biologically active FGF23 is glycosylation by the UDP-N-acetyl-α-D-galactosamine:polypeptide N-acetylgalactosaminyl transferase (ppGalNAc-T3). In the absence of glycosylation, FGF23 is processed into inactive N- and C-terminal proteins by a subtilisin proprotein convertase, probably furin. Normally, most if not all circulating FGF23 is intact. In FD, C-terminal levels are elevated, suggesting altered FGF23 processing. Altered processing in FD is the result of a cAMP-dependent, coordinated decrease in ppGalNAc-T3 and an increase in furin enzyme activity. These findings, and emerging data from other diseases, suggest regulation of FGF23 processing may be a physiologically important process.
Indexed as
Identifiers
What OpenQuestion holds
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.