ReviewFrontiers in endocrinology2018
FGF23 Actions on Target Tissues-With and Without Klotho.
Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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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.
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Who cites it
110 citing papers in PubMed, 195 citations in OpenAlex.
- Trial
- Association of fibroblast growth factor 23 and α-klotho in hemodialysis patients during administration of ferric citrate hydrate: post hoc analysis of ASTRIO study.BMC nephrology · 2021Trial
- High cut-off dialysis mitigates pro-calcific effects of plasma on vascular progenitor cells.Scientific reports · 2021Trial
- Molecular characterization of normal and physiologically suppressed human parathyroid glands at single-cell resolution.Journal of the Endocrine Society · 2026Article
- Tumor-induced osteomalacia caused by fibroblast growth factor 23 excess : Delayed diagnosis resulting from overlooked hypophosphatemia-A case report.Wiener klinische Wochenschrift · 2026Article
- Fibroblast Growth Factor 23 and Outcomes in Acute Heart Failure.Biomolecules · 2026Article
- Article
- Fibroblast Growth Factor 23 as a Prognostic Biomarker in Post-Myocardial Infarction Outcomes: Influence of Renal Function and Its Modulation by Klotho.Journal of the American Heart Association · 2026Article
- Review
- Unveiling the biochemical signature of tumor-induced osteomalacia: implications for distinguishing it from primary osteoporosis.Frontiers in endocrinology · 2026Article
- Calcimimetics and CaSR signaling in CKD-MBD: bone-immune-vascular crosstalk and therapeutic potential.Frontiers in immunology · 2026Review
- Reference intervals for intact FGF 23 in healthy Korean adults: lower concentrations in young adulthood require age-specific partitioning.Frontiers in endocrinology · 2026Article
- Disruption of the FGFR1-FGF23-Phosphate Axis and Targeted Therapy in a Murine Model of Osteoglophonic Dysplasia.bioRxiv : the preprint server for biology · 2025Article
- X-Linked Hypophosphatemia: Role of Fibroblast Growth Factor 23 on Human Skeletal Muscle-Derived Cells.Calcified tissue international · 2025Article
- Expression of FGF23 and α-KLOTHO in Normal Human Kidney Development and Congenital Anomalies of the Kidney and Urinary Tract (CAKUT).Biomolecules · 2025Article
- The Roxadustat (FG-4592) ameliorates tubulointerstitial fibrosis by promoting intact FGF23 cleavage.Cell communication and signaling : CCS · 2025Article
- Association Between Circulating Inflammatory Cytokines and Dentofacial Anomalies.International dental journal · 2025Article
- Involvement of ADAM17-Klotho Crosstalk in High Glucose-Induced Alterations of Podocyte Function.International journal of molecular sciences · 2025Article
- Renal aging and its consequences: navigating the challenges of an aging population.Frontiers in pharmacology · 2025Review
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
50 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fibroblast growth factor (FGF) 23 is a phosphaturic hormone whose physiologic actions on target tissues are mediated by FGF receptors (FGFR) and klotho, which functions as a co-receptor that increases the binding affinity of FGF23 for FGFRs. By stimulating FGFR/klotho complexes in the kidney and parathyroid gland, FGF23 reduces renal phosphate uptake and secretion of parathyroid hormone, respectively, thereby acting as a key regulator of phosphate metabolism. Recently, it has been shown that FGF23 can also target cell types that lack klotho. This unconventional signaling event occurs in an FGFR-dependent manner, but involves other downstream signaling pathways than in "classic" klotho-expressing target organs. It appears that klotho-independent signaling mechanisms are only activated in the presence of high FGF23 concentrations and result in pathologic cellular changes. Therefore, it has been postulated that massive elevations in circulating levels of FGF23, as found in patients with chronic kidney disease, contribute to associated pathologies by targeting cells and tissues that lack klotho. This includes the induction of cardiac hypertrophy and fibrosis, the elevation of inflammatory cytokine expression in the liver, and the inhibition of neutrophil recruitment. Here, we describe the signaling and cellular events that are caused by FGF23 in tissues lacking klotho, and we discuss FGF23's potential role as a hormone with widespread pathologic actions. Since the soluble form of klotho can function as a circulating co-receptor for FGF23, we also discuss the potential inhibitory effects of soluble klotho on FGF23-mediated signaling which might-at least partially-underlie the pleiotropic tissue-protective functions of klotho.
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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.