ArticleThe Journal of clinical investigation2007
The parathyroid is a target organ for FGF23 in rats.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 415 papers, 4 of them syntheses that pooled it.
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
415 citing papers in PubMed, 4 syntheses or guidelines pooled it, 948 citations in OpenAlex.
- Influence of Klotho Protein Levels in Obesity and Sarcopenia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Meta-analysis and systematic review: burosumab as a promising treatment for children with X-linked hypophosphatemia.Frontiers in endocrinology · 2024Pooled it
- Correlation Between Soluble Klotho and Vascular Calcification in Chronic Kidney Disease: A Meta-Analysis and Systematic Review.Frontiers in physiology · 2021Pooled it
- Correlation between SolubleBioMed research international · 2018Pooled it
- FGF23, Frailty, and Falls in SPRINT.Journal of the American Geriatrics Society · 2021Trial
- Molecular characterization of normal and physiologically suppressed human parathyroid glands at single-cell resolution.Journal of the Endocrine Society · 2026Article
- Estrogen protects female mice with chronic kidney disease from fibroblast growth factor 23-induced left ventricular hypertrophy.Kidney international · 2026Article
- Fibroblast growth factor 23 at the crossroads of mineral metabolism and bone disease.Current opinion in nephrology and hypertension · 2026Review
- Modeling Longitudinal Relationships Between CKD-MBD Biomarker Trajectories with Interpretable Machine Learning in a Large Prospective CKD Cohort.Journal of clinical medicine · 2026Article
- Fibroblast growth factor 23: Regulation, signalling and systemic links between bone, metabolism and inflammation.Molecular metabolism · 2026Review
- Associations Between Klotho/FGF-Related Protein Expression in Peripheral Blood Mononuclear Cells, Inflammation, and Muscle Function in Middle-Aged Adults with Obesity: A Pilot Study.International journal of molecular sciences · 2026Article
- Bone mineral loss damages renal tubules in mice.Communications biology · 2026Article
- A novel mutation in exon 18 ofThe Journal of international medical research · 2026Article
- Combination therapy with nutritional vitamin D and calcimimetics in secondary hyperparathyroidism: a mechanism-based approach to restoring PTH regulation.Frontiers in nutrition · 2026Review
- Hypoparathyroidism: a brief historical overview for clinicians.Frontiers in endocrinology · 2026Review
- Treatment with Minicircle DNA Expressing a FGF23 Fragment in a Clinically relevant Mouse Model of X-Linked Hypophosphatemic Rickets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gene therapy for hemoglobinopathies: Clinical trial results and biology of hematopoietic stem cell and the bone marrow niche.Cell reports. Medicine · 2025Review
- Six cases ofJBMR plus · 2025Article
- Hypermethylation of the p16Acta histochemica et cytochemica · 2025Article
- Effects of a high-fat diet on gut microbiota and possible implications for bone health in male Wistar rats.Lipids · 2025Article
355 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Phosphate homeostasis is maintained by a counterbalance between efflux from the kidney and influx from intestine and bone. FGF23 is a bone-derived phosphaturic hormone that acts on the kidney to increase phosphate excretion and suppress biosynthesis of vitamin D. FGF23 signals with highest efficacy through several FGF receptors (FGFRs) bound by the transmembrane protein Klotho as a coreceptor. Since most tissues express FGFR, expression of Klotho determines FGF23 target organs. Here we identify the parathyroid as a target organ for FGF23 in rats. We show that the parathyroid gland expressed Klotho and 2 FGFRs. The administration of recombinant FGF23 led to an increase in parathyroid Klotho levels. In addition, FGF23 activated the MAPK pathway in the parathyroid through ERK1/2 phosphorylation and increased early growth response 1 mRNA levels. Using both rats and in vitro rat parathyroid cultures, we show that FGF23 suppressed both parathyroid hormone (PTH) secretion and PTH gene expression. The FGF23-induced decrease in PTH secretion was prevented by a MAPK inhibitor. These data indicate that FGF23 acts directly on the parathyroid through the MAPK pathway to decrease serum PTH. This bone-parathyroid endocrine axis adds a new dimension to the understanding of mineral homeostasis.
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.