ArticleEndocrinology2014
Neither absence nor excess of FGF23 disturbs murine fetal-placental phosphorus homeostasis or prenatal skeletal development and mineralization.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 50 citations in OpenAlex.
- Management of X-Linked Hypophosphatemia During Pregnancy: Case Report and Literature Review.Calcified tissue international · 2026Review
- Expression of FGF23 and α-KLOTHO in Normal Human Kidney Development and Congenital Anomalies of the Kidney and Urinary Tract (CAKUT).Biomolecules · 2025Article
- Maternal excess dietary phosphate intake in the periconceptional period is a potential risk for mineral disorders in offspring mice.Scientific reports · 2025Article
- FGFR4 Is Required for Concentric Growth of Cardiac Myocytes during Physiologic Cardiac Hypertrophy.Journal of cardiovascular development and disease · 2024Article
- Full-term pregnancy despite severe hypophosphatemia caused by tumor-induced osteomalacia.Oxford medical case reports · 2024Article
- Article
- Mineral Metabolism in Children: Interrelation between Vitamin D and FGF23.International journal of molecular sciences · 2023Review
- Phosphate, Calcium, and Vitamin D: Key Regulators of Fetal and Placental Development in Mammals.Advances in experimental medicine and biology · 2022Review
- The role of biomineralization in disorders of skeletal development and tooth formation.Nature reviews. Endocrinology · 2021Review
- Hormonal regulation of biomineralization.Nature reviews. Endocrinology · 2021Review
- Maternal and fetal vitamin D and their roles in mineral homeostasis and fetal bone development.Journal of endocrinological investigation · 2021Review
- Consensus Recommendations for the Diagnosis and Management of X-Linked Hypophosphatemia in Belgium.Frontiers in endocrinology · 2021Review
- Murine Fetal Serum Phosphorus is Set Independent of FGF23 and PTH, Except in the Presence of Maternal Phosphate Loading.Endocrinology · 2021Article
- Placental Vascular Calcification and Cardiovascular Health: It Is Time to Determine How Much of Maternal and Offspring Health Is Written in Stone.Frontiers in physiology · 2018Article
- FGF23 Is Not Required to Regulate Fetal Phosphorus Metabolism but Exerts Effects Within 12 Hours After Birth.Endocrinology · 2017Article
- Novel anatomic adaptation of cortical bone to meet increased mineral demands of reproduction.Bone · 2016Article
- Current concepts in perinatal mineral metabolism.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2016Article
- The G protein α subunit variant XLαs promotes inositol 1,4,5-trisphosphate signaling and mediates the renal actions of parathyroid hormone in vivo.Science signaling · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblast growth factor-23 (FGF23) controls serum phosphorus largely through actions on the kidneys to excrete phosphorus and reduce calcitriol. Although these actions are well established in adults and children, the role that FGF23 plays in regulating fetal phosphorus metabolism has not been previously studied. We used several mouse models to study the effect of endogenous deficiency or excess of FGF23 on fetal phosphorus metabolism. We found that intact FGF23 does not cross the placenta from mother to fetus, but wild-type fetuses normally have intact FGF23 levels that approximately equal the maternal level. Deletion of Fgf23 or 7.8-fold higher serum FGF23 levels did not disturb any parameter of fetal mineral homeostasis, including serum and amniotic fluid phosphorus, skeletal morphology, skeletal mineral content, and placental phosphorus transport. Placentas and fetal kidneys abundantly express FGF23 target genes. Cyp24a1 was significantly reduced in Fgf23 null kidneys and was significantly increased in Phex null placentas and fetal kidneys. Phex null kidneys also showed reduced expression of Klotho. However, these changes in gene expression did not disturb any physiological parameter related to phosphorus. A 50% reduction in FGF23 also failed to affect renal phosphorus excretion into amniotic fluid when either PTH or the vitamin D receptor were absent. In conclusion, FGF23 is not an important regulator of fetal phosphorous metabolism. The active delivery of phosphorus across the placenta does not require FGF23, and that process overrides any effects that absence or excess of FGF23 might otherwise have on phosphate handling by the fetal kidneys.
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Registered trials
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