ReviewCurrent osteoporosis reports2014
Hypophosphatemic rickets: revealing novel control points for phosphate homeostasis.
Review in Current osteoporosis reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 34 citations in OpenAlex.
- Effect of ferric citrate on serum phosphate and fibroblast growth factor 23 among patients with nondialysis-dependent chronic kidney disease: path analyses.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2019Trial
- A Diagnostic Dilemma: Hypophosphatemic Rickets Unmasking Tyrosinemia Type 1: A Case Report.Clinical case reports · 2026Article
- Longitudinal Single-Cell Transcriptomic Profiling Reveals Dynamic Immune Cell Alterations During Burosumab Therapy in X-Linked Hypophosphatemia.Pediatric discovery · 2026Article
- Regulation of secretory pathway kinase or kinase-like proteins in human cancers.Frontiers in immunology · 2023Review
- Perioperative changes of FGF23 in patients undergoing surgery for primary hyperparathyroidism.Endocrine connections · 2022Article
- A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo.Endocrinology · 2019Article
- Expression and function of Slc34 sodium-phosphate co-transporters in skeleton and teeth.Pflugers Archiv : European journal of physiology · 2019Review
- Dentoalveolar Abscesses Not Associated with Caries or Trauma: A Diagnostic Hallmark of Hypophosphatemic Rickets Initially Misdiagnosed as Hypochondroplasia.Head and neck pathology · 2018Article
- Role of phosphate sensing in bone and mineral metabolism.Nature reviews. Endocrinology · 2018Review
- The Association Between Fibroblast Growth Factor 23 and Renal Transplantation Outcome Is Modified by Follow-up Duration and Glomerular Filtration Rate Assessment Method.Kidney international reports · 2017Article
- Skeletal Muscle, but not Cardiovascular Function, Is Altered in a Mouse Model of Autosomal Recessive Hypophosphatemic Rickets.Frontiers in physiology · 2016Article
- The secretory pathway kinases.Biochimica et biophysica acta · 2015Review
- Fibroblast growth factor signaling in skeletal development and disease.Genes & development · 2015Review
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 2 institutions in 1 country.
Funding
Abstract
Rapid and somewhat surprising advances have recently been made toward understanding the molecular mechanisms causing heritable disorders of hypophosphatemia. The results of clinical, genetic, and translational studies have interwoven novel concepts underlying the endocrine control of phosphate metabolism, with far-reaching implications for treatment of both rare Mendelian diseases as well as common disorders of blood phosphate excess such as chronic kidney disease (CKD). In particular, diseases caused by changes in the expression and proteolytic control of the phosphaturic hormone fibroblast growth factor-23 (FGF23) have come to the forefront in terms of directing new models explaining mineral metabolism. These hypophosphatemic disorders as well as others resulting from independent defects in phosphate transport or metabolism will be reviewed herein, and implications for emerging therapeutic strategies based upon these new findings will be discussed.
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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.